ascorbic-acid and Myocardial-Ischemia
ascorbic-acid has been researched along with Myocardial-Ischemia* in 59 studies
Reviews
5 review(s) available for ascorbic-acid and Myocardial-Ischemia
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Identification and quantification of free radicals during myocardial ischemia and reperfusion using electron paramagnetic resonance spectroscopy.
There is general agreement that free radicals are involved in reperfusion injury. Electron paramagnetic resonance (EPR) spectroscopy can be considered as the more suitable technique to directly measure and characterize free radical generation during myocardial ischemia and reperfusion. There are essentially two approaches used in the detection of unstable reactive species: freezing technique and spin traps. The detection of secondary free radicals or ascorbyl free radicals during reperfusion might provide an index of oxidative stress. Spin trapping can also characterize nitric oxide. EPR spectroscopy can provide important data regarding redox state and free radical metabolism but ideally, the spin traps must not interfere with cell or organism function. Topics: Animals; Ascorbic Acid; Electron Spin Resonance Spectroscopy; Free Radicals; Freezing; Humans; Myocardial Ischemia; Myocardial Reperfusion; Myocardial Reperfusion Injury; Nitric Oxide; Oxidation-Reduction; Oxidative Stress; Spin Trapping | 2003 |
Beta-carotene, vitamin C, and vitamin E and cardiovascular diseases.
Observational studies have shown an inverse relationship between consumption of fruits and vegetables high in beta-carotene, vitamins C and E, and ischemic heart disease (IHD) and stroke. In large observational studies, beta- carotene reduced the risk of IHD events in men, particularly in smokers. In contrast, four large randomized trials did not reveal a reduction in cardiovascular events with beta-carotene use, and may, in fact, increase IHD and total mortality in male smokers. There have been only a few large observational studies and one randomized trial with vitamin C, which have shown no beneficial or deleterious impact of this vitamin on cardiovascular events. Most large observational studies have shown an inverse relationship between vitamin E and IHD. However, a meta-analysis of the four randomized trials done in Europe and America involving a total of 51,000 participants allocated to vitamin E or placebo for 1.4 to 6 years, did not demonstrate a reduction in cardiovascular and IHD mortality and nonfatal myocardial infarction. Currently, there are no data to support the use of these vitamins to reduce the risk of cardiovascular events. Trials are in progress to determine whether a longer duration of administration of vitamin E or the association of vitamin E with cofactors may reduce cardiovascular events. Topics: Animals; Antioxidants; Ascorbic Acid; beta Carotene; Cardiovascular Diseases; Dietary Supplements; Endothelium, Vascular; Humans; Male; Myocardial Ischemia; Randomized Controlled Trials as Topic; Vitamin E | 2000 |
By how much does fruit and vegetable consumption reduce the risk of ischaemic heart disease?
To quantify the relationship between fruit and vegetable consumption and the incidence of ischaemic heart disease.. A meta-analysis of cohort studies of the relationship between ischaemic heart disease and markers of fruit and vegetable consumption, namely dietary intake of fruit, vegetables, carotenoids, vitamin C, fruit fibre and vegetable fibre, and serum concentration of carotenoids and vitamin C, adjusted for other risk factors.. Risk of ischaemic heart disease at the 90th centile of consumption relative to that at the 10th, equivalent to about a four-fold difference in fruit consumption and a doubling of vegetable consumption.. The association with ischaemic heart disease was of similar magnitude for all six dietary markers of fruit and vegetable consumption. The median of the six estimates was that risk was 15% (range 12-19%) lower at the 90th centile of consumption than at the 10th. The estimates were generally adjusted for the possible confounding effect of other heart disease risk factors. The serum studies of vitamin C were consistent with this; those of carotenoids suggested a larger difference (43%) but were not adjusted for the important confounding effect of smoking. The substances in fruit and vegetables responsible for the protective effect on heart disease are uncertain but the effect is commensurate with the estimated protective effects of the potassium and folate in fruit and vegetables. Beta-carotene or vitamin E are not likely to be important because randomised trials of these vitamins in large doses have shown no reduction in heart disease mortality.. The risk of ischaemic heart disease is about 15% lower at the 90th than the 1Oth centile of fruit and vegetable consumption. Topics: Adult; Aged; Ascorbic Acid; Biomarkers; Carotenoids; Cohort Studies; Diet; Dietary Fiber; Female; Folic Acid; Fruit; Humans; Male; Middle Aged; Myocardial Ischemia; Potassium; Vegetables | 1998 |
Free radical scavenging and antioxidant activity of plant flavonoids.
Topics: Animals; Antioxidants; Ascorbic Acid; Coronary Disease; Drug Interactions; Flavonoids; Free Radical Scavengers; Free Radicals; Humans; Lipid Peroxidation; Molecular Structure; Myocardial Ischemia; Myocardial Reperfusion; Oxidation-Reduction; Phagocytes; Plants; Reactive Oxygen Species | 1994 |
Increased risk of cardiovascular disease at suboptimal plasma concentrations of essential antioxidants: an epidemiological update with special attention to carotene and vitamin C.
For the prolongation of life expectancy and reduction of ischemic heart disease (IHD) dietary guidelines generally recommend lowering saturated mammalian fat with partial replacement by vegetable oils and increasing generously vegetables, legumes, and fruits, which provide more essential antioxidants. Plasma antioxidants as assayed in epidemiological studies of complementary type (ie the cross-cultural MONICA Vitamin Substudy reevaluation considering the "Finland-Factor", the Edinburgh Angina-Control Study, and the Basel Prospective Study) consistently revealed an increased risk of IHD (and stroke) at low plasma concentrations of antioxidants, with the rank order as follows: lipid-standardized vitamin E >> carotene = vitamin C > vitamin A, independently of classical IHD risk factors. Decreasing IHD risk through nutrition may be possible when plasma concentrations have the following values: > 27.5-30.0 mumol vitamin E/L, 0.4-0.5 mumol carotene/L, 40-50 mumol vitamin C/L and 2.2-2.8 mumol vitamin A/L. Thus, previous prudent regimens may now be updated, aiming at an optimal status of all essential and synergistically linked antioxidants. Topics: Angina Pectoris; Ascorbic Acid; Blood Pressure; Carotenoids; Cerebrovascular Disorders; Cholesterol; Cross-Cultural Comparison; Humans; Male; Middle Aged; Myocardial Ischemia; Risk Factors; Selenium; Vitamin E | 1993 |
Trials
12 trial(s) available for ascorbic-acid and Myocardial-Ischemia
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Therapeutic role of L-arginine on free radical scavenging system in ischemic heart diseases.
Increased production of free radicals under oxidative stress conditions plays a vital role in the impairment of endothelial function and also in the pathogenesis of ischemic heart diseases. Ischemia, followed by reperfusion, leads to the exacerbated formation of oxy- free radicals. These reactive oxygen species through a chain of reactions damage the cardiomyocytes and cause more injury to the myocardium. L-Arginine is reported to act as free radical scavenger, inhibits the activity of pro-oxidant enzymes and thus acts as an antioxidant and these roles of L-arginine are mediated by nitric oxide (NO). In the present study, the effect of oral administration of L-arginine (3 g/day for 7 days) on some antioxidant enzymes, total thiols, lipid peroxidation measured as malondialdehyde (MDA), and plasma ascorbate levels in myocardial ischemic patients was investigated. We observed an increase in the activity of superoxide dismutase (SOD), total thiols (T-SH) and plasma ascorbate levels and a decrease in the activity of xanthine oxidase (XO), MDA levels, carbonyl content and serum cholesterol in the patients on oral administration of L-arginine. The present study demonstrates that L-arginine administration may be beneficial to patients with myocardial ischemic disorders, such as acute myocardial infarction and acute angina. Topics: Adult; Aged; Arginine; Ascorbic Acid; Case-Control Studies; Cholesterol; Free Radical Scavengers; Humans; Malondialdehyde; Middle Aged; Myocardial Ischemia; Oxidants; Sulfhydryl Compounds; Superoxide Dismutase; Xanthine Oxidase | 2009 |
Effect of hyperoxia and vitamin C on coronary blood flow in patients with ischemic heart disease.
Pathological formation of reactive oxygen species within the coronary circulation has been hypothesized to mediate some clinical manifestations of ischemic heart disease (IHD) by interfering with physiological regulation of coronary tone. To determine the degree to which coronary tone responds to acute changes in ambient levels of oxidants and antioxidants in vivo in a clinical setting, we measured the effect of an acute oxidative stress (breathing 100% oxygen) on coronary capacitance artery diameter (quantitative angiography) and blood flow velocity through the coronary microcirculation (intracoronary Doppler ultrasonography) before and after treatment with the antioxidant vitamin C (3-g intravenous infusion) in 12 IHD patients undergoing a clinical coronary interventional procedure. Relative to room air breathing, 100% oxygen breathing promptly reduced coronary blood flow velocity by 20% and increased coronary resistance by 23%, without significantly changing the diameter of capacitance arteries. Vitamin C administration promptly restored coronary flow velocity and resistance to a slightly suprabasal level, and it prevented the reinduction of coronary constriction with rechallenge with 100% oxygen. This suggests that acute oxidative stress produces prompt and substantial changes in coronary resistance and blood flow in a clinical setting in patients with IHD, and it suggests that these changes are mediated by vitamin C-quenchable substances acting on the coronary microcirculation. This observation may have relevance for clinical practice. Topics: Aged; Antioxidants; Ascorbic Acid; Blood Flow Velocity; Coronary Angiography; Coronary Circulation; Coronary Vessels; Female; Humans; Hyperoxia; Infusions, Intravenous; Laser-Doppler Flowmetry; Male; Middle Aged; Myocardial Ischemia; Oxidative Stress; Vascular Resistance | 2007 |
Effect of intensive lipid lowering, with or without antioxidant vitamins, compared with moderate lipid lowering on myocardial ischemia in patients with stable coronary artery disease: the Vascular Basis for the Treatment of Myocardial Ischemia Study.
Lipid lowering with statins prevents adverse cardiac events. Both lipid-lowering and antioxidant therapies may favorably affect vasomotor function and thereby improve ischemia.. In a randomized, double-blind, placebo-controlled trial, 300 patients with stable coronary disease, a positive exercise treadmill test, 48-hour ambulatory ECG with > or =1 episode of ischemia, and fasting total cholesterol of 180 to 250 mg/dL were assigned to 1-year treatment with intensive atorvastatin to reduce LDL to <80 mg/dL (n=96), intensive atorvastatin to reduce LDL to <80 mg/dL plus antioxidant vitamins C (1000 mg/d) and E (800 mg/d) (n=101), or diet and low-dose lovastatin, if needed, to reduce LDL to <130 mg/dL (n=103; control group). Ischemia end points, including ambulatory ECG monitoring and exercise treadmill testing, and endothelial assessment using brachial artery flow-mediated dilation were obtained at baseline and at 6 and 12 months. Baseline characteristics were similar in all groups. LDL decreased from approximately 153 mg/dL at baseline in the 2 atorvastatin groups to approximately 83 mg/dL at 12 months (each P<0.0001) and from 147 to 120 mg/dL in the control group (P<0.0001). During ambulatory ECG monitoring, mean number of ischemic episodes per 48 hours decreased 31% to 61% in each group (each P<0.001; P=0.15 across groups), without a change in daily heart rate activity. Mean duration of ischemia for 48 hours decreased 26% to 62% in each group (each P<0.001; P=0.06 across groups). Mean exercise duration to 1-mm ST-segment depression significantly increased in each group, but total exercise duration and mean sum of maximum ST depression were unchanged. Angina frequency decreased in each group. There was no incremental effect of supplemental vitamins C and E on any ischemia outcome. Flow-mediated dilation studies indicated no meaningful changes.. Intensive lipid lowering with atorvastatin to an LDL level of 80 mg/dL, with or without antioxidant vitamins, does not provide any further benefits in ambulatory ischemia, exercise time to onset of ischemia, and angina frequency than moderate lipid lowering with diet and low-dose lovastatin to an LDL level of <120 mg/dL. Topics: Angina Pectoris; Antioxidants; Ascorbic Acid; Atorvastatin; Coronary Artery Disease; Diet Therapy; Dose-Response Relationship, Drug; Exercise Test; Female; Heptanoic Acids; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Lipid Metabolism; Lipids; Lipoproteins, LDL; Male; Myocardial Ischemia; Pyrroles; Vasomotor System; Vitamin E | 2005 |
Influence of L-arginine and vitamin C on the autonomic nervous system in chronic heart failure secondary to ischemic cardiomyopathy.
In this study, we used spectral analysis to assess changes in respiratory recording variability during infusion of L-arginine and vitamin C, individually or together, in patients with chronic heart failure. We found that healthy subjects have a substantial ability to modulate sympathetic-mediated peripheral vascular resistance through endothelial synthesis of nitric oxide. Patients with chronic heart failure lose this ability. Topics: Algorithms; Antioxidants; Arginine; Ascorbic Acid; Autonomic Nervous System; Cardiomyopathy, Dilated; Cross-Over Studies; Female; Humans; Male; Middle Aged; Myocardial Ischemia; Respiration; Signal Processing, Computer-Assisted; Single-Blind Method; Vascular Resistance | 2004 |
Vascular basis for the treatment of myocardial ischemia study: trial design and baseline characteristics.
Increased low-density lipoprotein (LDL) and oxidized LDL cholesterol levels adversely affect endothelial function in patients with stable coronary artery disease (CAD). Statin drugs are efficacious in primary and secondary prevention of clinical CAD events, but they have not been extensively studied as a treatment for ischemia during routine daily activities or during exercise, indicators of high-risk in patients with stable CAD. The purpose of the Vascular Basis for the Treatment of Myocardial Ischemia study is to determine whether aggressive lowering of LDL cholesterol level with atorvastatin, with or without supplemental antioxidant vitamins C and E, can improve endothelial function and ischemia during ambulatory electrocardiogram (AECG) monitoring and exercise treadmill testing (ETT).. Patients are eligible when they have ischemia during an ETT and AECG monitoring and when their fasting total cholesterol level is < or =250 mg/dL. Eligible patients are randomized to receive 1 of 3 treatments: intensive atorvastatin to reduce LDL cholesterol level to < or =80 mg/dL, intensive atorvastatin to reduce LDL cholesterol level to < or =80 mg/dL plus antioxidant vitamins C and E, and control of diet and low-dose lovastatin, when needed, to reduce LDL cholesterol level < or = to 130 mg/dL. Patients undergo endothelial function testing, 48-hour AECG monitoring, and ETT at randomization and at 6 and 12 months.. A total of 300 patients have been randomized: 101 to receive atorvastatin alone, 103 to receive atorvastatin plus antioxidant vitamins, and 96 to receive placebo. Baseline characteristics are similar across treatment groups.. The Vascular Basis study will provide important insight on the effects of aggressive management of dyslipidemia with statin drugs and antioxidant vitamins in patients with stable but high-risk CAD. Topics: Adult; Aged; Aged, 80 and over; Anticholesteremic Agents; Antioxidants; Ascorbic Acid; Atorvastatin; Brachial Artery; Cholesterol, LDL; Double-Blind Method; Female; Heptanoic Acids; Humans; Male; Middle Aged; Myocardial Ischemia; Pyrroles; Regional Blood Flow; Ultrasonography; Vasodilation; Vitamin E | 2004 |
The SU.VI.MAX Study: a randomized, placebo-controlled trial of the health effects of antioxidant vitamins and minerals.
It has been suggested that a low dietary intake of antioxidant vitamins and minerals increases the incidence rate of cardiovascular disease and cancer. To date, however, the published results of randomized, placebo-controlled trials of supplements containing antioxidant nutrients have not provided clear evidence of a beneficial effect. We tested the efficacy of nutritional doses of supplementation with a combination of antioxidant vitamins and minerals in reducing the incidence of cancer and ischemic cardiovascular disease in the general population.. The Supplementation en Vitamines et Mineraux Antioxydants (SU.VI.MAX) study is a randomized, double-blind, placebo-controlled primary prevention trial. A total of 13 017 French adults (7876 women aged 35-60 years and 5141 men aged 45-60 years) were included. All participants took a single daily capsule of a combination of 120 mg of ascorbic acid, 30 mg of vitamin E, 6 mg of beta carotene, 100 mug of selenium, and 20 mg of zinc, or a placebo. Median follow-up time was 7.5 years.. No major differences were detected between the groups in total cancer incidence (267 [4.1%] for the study group vs 295 [4.5%] for the placebo group), ischemic cardiovascular disease incidence (134 [2.1%] vs 137[2.1%]), or all-cause mortality (76 [1.2%] vs 98 [1.5%]). However, a significant interaction between sex and group effects on cancer incidence was found (P = .004). Sex-stratified analysis showed a protective effect of antioxidants in men (relative risk, 0.69 [95% confidence interval [CI], 0.53-0.91]) but not in women (relative risk, 1.04 [95% CI, 0.85-1.29]). A similar trend was observed for all-cause mortality (relative risk, 0.63 [95% CI, 0.42-0.93] in men vs 1.03 [95% CI, 0.64-1.63] in women; P = .11 for interaction).. After 7.5 years, low-dose antioxidant supplementation lowered total cancer incidence and all-cause mortality in men but not in women. Supplementation may be effective in men only because of their lower baseline status of certain antioxidants, especially of beta carotene. Topics: Adult; Antioxidants; Ascorbic Acid; beta Carotene; Dietary Supplements; Female; Follow-Up Studies; Humans; Male; Middle Aged; Myocardial Ischemia; Neoplasms; Selenium; Vitamin E; Zinc | 2004 |
[The study of the clinical potency of antiatherogenic diet containing flavonoids in cardiovascular patients].
At 60 patients with coronary artery disease and high blood pressure studied effects of a diet with low lipid and flavons. The application of a diet and flavons promoted positive dynamics (changes) of clinical manifestations of disease, lipid spectrum and antioxidants. Topics: Adult; Aged; Antioxidants; Arteriosclerosis; Ascorbic Acid; Cardiovascular Diseases; Diet; Electrocardiography; Flavonoids; Humans; Hypertension; Lipid Peroxidation; Malondialdehyde; Middle Aged; Myocardial Ischemia; Obesity | 2003 |
Improvement of peripheral endothelial dysfunction by acute vitamin C application: different effects in patients with coronary artery disease, ischemic, and dilated cardiomyopathy.
Endothelial dysfunction has been described in patients with coronary artery disease (CAD) or chronic heart failure (CHF). Vitamin C administration leads to an improvement of endothelial function by reducing elevated levels of reactive oxygen species. It remains unclear, however, whether the degree of endothelial dysfunction caused by oxidative stress differs between CAD and CHF because of ischemic (ICM) or dilated cardiomyopathy (DCM).. In patients with CAD (n = 9; left ventricular ejection fraction [LVEF], 64% +/- 3%), ICM (n = 9; LVEF, 25% +/- 4%), DCM (n = 9; LVEF, 25% +/- 3%), and healthy subjects (HS; n = 5; LVEF, 66% +/- 5%) a change in internal radial artery diameter in response to acetylcholine (Ach; 15 and 30 microg/min) was measured with high-resolution ultrasound scanning during a co-infusion of normal saline or vitamin C (25 mg/min).. Ach-mediated vasodilation was blunted in patients with CHF (DCM, 90 +/- 20 microm; ICM, 86 +/- 20 microm) and patients with CAD (336 +/- 20 microm) as compared with HS (496 +/- 43 microm; P <.05 vs patients with DCM, ICM, CAD). Vitamin C co-infusion increased Ach-mediated vasodilation by 180 +/- 35 microm (to 270 +/- 30 microm) in DCM (P <.05 vs CAD, HS) and by 294 +/- 40 microm (to 380 +/- 20 microm) in ICM (P <.05 vs DCM, CAD, HS). In patients with CAD, vitamin C increased Ach-mediated vasodilation by 146 +/- 35 microm to normal values, whereas vascular diameter remained unchanged in HS (14 +/- 20 microm; P = not significant).. Acute vitamin C administration restored peripheral endothelial function in patients with CAD to normal values, whereas endothelial function remained attenuated in CHF, in particular in patients with DCM. These results suggest that in patients with CHF, factors other than oxidative stress (eg, cytokines) contribute to the pathologic endothelial function. Topics: Acetylcholine; Aged; Ascorbic Acid; Cardiomyopathy, Dilated; Chronic Disease; Coronary Artery Disease; Drug Therapy, Combination; Endothelium, Vascular; Heart Failure; Humans; Male; Middle Aged; Myocardial Ischemia; Nitroprusside; Oxidative Stress; Vasodilation; Vasodilator Agents | 2003 |
[Use of ascorbic acid for raising clinical response to long-acting nitrates].
The data of clinic observation and ECG-monitoring show that ascorbic acid significantly increases antianginal vasodilatory effects of nitroglycerine thus preventing from development of ischemic miocardial reaction in response to complamin injection. Incubation under anaerobe conditions of ascorbic acid solution with NO-donors (sodium nitrate, nitroglycerine) or with the blood of ischemic patients who had been treated for a long time with long-acting nitrovasodilators, results in liberation in Varburg vasculium of gas bubbles identified as nitrogen oxide according to hemoglobin nitrosylation. Activation of endogen NO-donors with ascorbic acid and taking antilogs of antianginal effects of exogenous nitroglycerine makes it possible to substantially increase the efficiency of nitratotherapy and nitratoprophylaxis of angina pectoris. Topics: Adult; Aged; Ascorbic Acid; Drug Synergism; Humans; Male; Middle Aged; Myocardial Ischemia; Nitro Compounds; Vasodilator Agents | 2002 |
[Cortisol levels in blood of persons with acute myocardial ischemia and myocardial infarction].
An increase in blood level of Cortisol and overproduction of free radicals is present during first days following acute ischemia and myocardial infarction. This increase exceeds the activity of protective compounds and systems of myocardial cells undergoing ischemia. The aim of this work was to study the relationship between the Cortisol blood level and the intensity of free radical reactions in patients with acute myocardial ischemia and acute myocardial infarction with respect to metabolic (glucose, uric acid) and enzymatic agents of ischemia and necrosis. The study was performed in 75 patients (20 females and 55 males) aged 38-75 years, including 13 patients with acute myocardial ischemia (6 females and 7 males) aged 40-66 years (group I), 40 patients with acute myocardial infarction (8 females and 32 males) aged 38-72 years (group II) and 22 healthy volunteers (6 females and 16 males) aged 39-75 years (control group). The concentration of Cortisol in blood and other biochemical determinants were measured on the second, fifth and seventh day following admission to the coronary care unit. The intensity of free radicals reactions was measured by using the concentration of Vitamin C, malondialdehyde (MDA), uric acid and white blood cells (WBC) count as markers. The results obtained have led to the following conclusions: 1. The increase in blood level of Cortisol in acute myocardial infarction is higher in comparison to the level of Cortisol in acute myocardial ischemia. 2. The intensity of free radical reactions during acute myocardial ischemia and acute myocardial infarction can be assessed by the decreased level of Vitamin C, increased level of malondialdehyde, uric acid concentration and leukocyte (WBC) count. 3. There is no correlation between the intensity of free radical reactions and elevation of blood cortisol during both acute myocardial ischemia and acute myocardial infarction. 4. Elevated levels of Cortisol in blood correlate with elevated levels of glucose and uric acid in blood during both acute myocardial ischemia and acute myocardial infarction. 5. Increase in enzymatic markers of ischemia and necrosis during acute myocardial ischemia and necrosis shows no correlation with the intensity of free radicals reactions. Topics: Adult; Aged; Ascorbic Acid; Female; Free Radicals; Humans; Hydrocortisone; Leukocyte Count; Male; Malondialdehyde; Middle Aged; Myocardial Infarction; Myocardial Ischemia; Uric Acid | 1999 |
[The influence of vitamin C and e or beta-carotene on peroxidative processes in persons with myocardial ischemia].
An increasing body of evidence suggests that beside hypercholesterolemia peroxidative processes and natural antioxidant defence system play important role in the development of atherosclerosis. Our earlier investigation showed the increased intensity of the peroxidative processes in the course of the acute myocardial infarction and unsatisfactory tocopherol, ascorbic acid and retinol status. The purpose of the present study was the evaluation of the effect of antioxidant vitamins supplementation by the period of 21 days on the peroxidative processes in patients after heart attack or after "bypass" admitted to the cardiological rehabilitation centre. Daily oral supplementation with vitamin C, E and beta-carotene decreased significantly plasma lipid peroxide concentration (TBARS). The highest drop in TBARS activity was found in the group after bypass. No significant effect of vitamin supplementation was observed on antioxidant enzymes activity. Topics: Aged; Antioxidants; Ascorbic Acid; beta Carotene; Coronary Artery Bypass; Dietary Supplements; Female; Humans; Lipid Peroxides; Male; Middle Aged; Myocardial Ischemia; Vitamin E | 1998 |
Randomized, double-blind, placebo-controlled study of the preventive effect of supplemental oral vitamin C on attenuation of development of nitrate tolerance.
This study sought to evaluate the preventive effect of vitamin C, an antioxidant, on the development of nitrate tolerance.. Decreased intracellular production of cyclic guanosine monophosphate (cGMP) is a mechanism of nitrate tolerance, and increased superoxide levels and reduced activation of guanylate cyclase have been observed in vitro.. In this double-blind, placebo-controlled study, 24 normal volunteers and 24 patients with ischemic heart disease (IHD) were randomized to receive either vitamin C (2 g three times daily [vitamin C group, n=12]) or placebo (placebo group, n=12). The vasodilator response to nitroglycerin was assessed with forearm plethysmography by measuring the change in FBF before and 5 min after sublingual administration of 0.3 mg of nitroglycerin. Blood samples were simultaneously obtained to measure platelet cGMP levels. FBF was measured, and blood sampling was performed serially at baseline (day 0), 3 days after administration of vitamin C or placebo (day 3) and 3 days after application of a 10-mg/24-h nitroglycerin tape concomitantly with oral vitamin C or placebo (day 6).. There were no differences between the vitamin C and placebo groups in percent increases in FBF (%FBF) or platelet cGMP levels (%cGMP) after administration of sublingual nitroglycerin on day O (%FBF: normal volunteers 31+/-8 vs. 32+/-10; patients with IHD 32+/-9 vs. 32+/-8; %cGMP: normal volunteers 37+/-9 vs. 39+/-10; patients with IHD 38+/-10 vs. 39+/-10 [vitamin C group vs. placebo group]) or day 3 (%FBF: normal volunteers 32+/-9 vs. 33+/-9; patients with IHD 31+/-10 vs. 31+/-10; %cGMP: normal volunteers 36+/-8 vs. 37+/-9; patients with IHD 39+/-11 vs. 38+/-10 [vitamin C group vs. placebo group]). The %FBF and %cGMP in the placebo group were significantly lower on day 6 than in the vitamin C group (%FBF: normal volunteers 30+/-8 vs. 19 4, p < 0.01; patients with IHD 29+/-9 vs. 17+/-6, p < 0.01; %cGMP: normal volunteers 36 10 vs. 17+/-6, p < 0.01; patients with IHD 37+/-11 vs. 15+/-5, p < 0.01 [vitamin C group vs. placebo group]).. These results indicate that combination therapy with vitamin C is potentially useful for preventing the development of nitrate tolerance. Topics: Adult; Aged; Antioxidants; Ascorbic Acid; Cyclic GMP; Double-Blind Method; Drug Therapy, Combination; Drug Tolerance; Female; Humans; Male; Middle Aged; Myocardial Ischemia; Nitroglycerin; Plethysmography; Vasodilator Agents | 1998 |
Other Studies
42 other study(ies) available for ascorbic-acid and Myocardial-Ischemia
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Assessment of Vitamin C and Antioxidant Profiles in Saliva and Serum in Patients with Periodontitis and Ischemic Heart Disease.
Vitamin C and antioxidants play a crucial role in endothelial function and may be a link for the known interaction of periodontitis and ischemic heart disease (CAD). This pilot study evaluates the association of gingival health, periodontitis, CAD, or both conditions with salivary and serum vitamin C and antioxidant levels. The clinical and periodontal characteristics, serum, and saliva samples were collected from 36 patients with periodontitis, 35 patients with CAD, 36 patients with periodontitis plus CAD, and 36 healthy controls. Levels of vitamin C, antioxidants, and C-reactive protein (hs-CRP) were assessed with a commercially available kit. The median concentrations of salivary and serum vitamin C and antioxidants (α-tocopherol, β-carotene, lutein, and lycopene) were significantly lower in the CAD group ( Topics: Adult; Antioxidants; Ascorbic Acid; Case-Control Studies; Humans; Middle Aged; Myocardial Ischemia; Periodontitis; Saliva | 2019 |
Attenuation of atherogenic apo B-48-dependent hyperlipidemia and high density lipoprotein remodeling induced by vitamin C and E combination and their beneficial effect on lethal ischemic heart disease in mice.
Atherosclerotic cardiovascular disease is highly prevalent and its underlying pathogenesis involves dyslipidemia including pro-atherogenic high density lipoprotein (HDL) remodeling. Vitamins C and E have been proposed as atheroprotective agents for cardiovascular disease management. However, their effects and benefits on high density lipoprotein function and remodeling are unknown. In this study, we evaluated the role of vitamin C and E on non HDL lipoproteins as well as HDL function and remodeling, along with their effects on inflammation/oxidation biomarkers and atherosclerosis in atherogenic diet-fed SR-B1 KO/ApoER61. Mice were pre-treated for 5 weeks before and during atherogenic diet feeding with vitamin C and E added to water and diet, respectively. Compared to a control group, combined vitamin C and E administration reduced serum total cholesterol and triglyceride levels by decreasing apo B-48-containing lipoproteins, remodeled HDL particles by reducing phospholipid as well as increasing PON1 and apo D content, and diminished PLTP activity and levels. Vitamin supplementation improved HDL antioxidant function and lowered serum TNF-α levels. Vitamin C and E combination attenuated atherogenesis and increased lifespan in atherogenic diet-fed SR-B1 KO/ApoER61. Vitamin C and E administration showed significant lipid metabolism regulating effects, including HDL remodeling and decreased levels of apoB-containing lipoproteins, in mice. In addition, this vitamin supplementation generated a cardioprotective effect in a murine model of severe and lethal atherosclerotic ischemic heart disease. Topics: Animals; Antioxidants; Apolipoprotein B-48; Ascorbic Acid; Cardiotonic Agents; Coronary Artery Disease; Cytokines; Diet, Atherogenic; Dietary Supplements; Enzyme-Linked Immunosorbent Assay; Female; Hyperlipidemias; Immunoblotting; Lipid Metabolism; Lipoproteins, HDL; Male; Mice, Inbred C57BL; Myocardial Ischemia; Phospholipid Transfer Proteins; Reference Values; Reproducibility of Results; Scavenger Receptors, Class B; Treatment Outcome; Vitamin E | 2018 |
Genetically high plasma vitamin C, intake of fruit and vegetables, and risk of ischemic heart disease and all-cause mortality: a Mendelian randomization study.
High intake of fruit and vegetables as well as high plasma vitamin C concentrations have been associated with low risk of ischemic heart disease in prospective studies, but results from randomized clinical trials have been inconsistent.. We tested the hypothesis that genetically high concentrations of plasma vitamin C, such as with high intake of fruit and vegetables, are associated with low risk of ischemic heart disease and all-cause mortality.. We used a Mendelian randomization approach and genotyped for solute carrier family 23 member 1 (SLC23A1) rs33972313 in the sodium-dependent vitamin C transporter 1 in 97,203 white individuals of whom 10,123 subjects had ischemic heart disease, and 8477 subjects died. We measured plasma vitamin C in 3512 individuals and included dietary information on 83,256 individuals.. The SLC23A1 rs33972313 G allele was associated with 11% higher plasma vitamin C. The multivariable adjusted HRs for highest compared with lowest fruit and vegetable intakes were 0.87 (95% CI: 0.78, 0.97; P = 0.01) for ischemic heart disease and 0.80 (95% CI: 0.73, 0.88; P < 0.001) for all-cause mortality. Corresponding HRs for rs33972313 GG (93%) compared with AA plus AG (7%) genotypes were 0.95 (95% CI: 0.88, 1.02; P = 0.21) and 0.96 (0.88, 1.03; P = 0.29), respectively. In an instrumental variable analysis, the OR for genetically determined 25% higher plasma vitamin C concentrations was 0.90 (95% CI: 0.75, 1.08; P = 0.27) for ischemic heart disease and 0.88 (0.72, 1.08; P = 0.22) for all-cause mortality.. High intake of fruit and vegetables was associated with low risk of ischemic heart disease and all-cause mortality. Although the 95% CI for genetically high plasma vitamin C concentrations overlapped 1.0, which made certain statistical inferences difficult, effect sizes were comparable to those for fruit and vegetable intake. Thus, judging by the effect size, our data cannot exclude that a favorable effect of high intake of fruit and vegetables could in part be driven by high vitamin C concentrations. Topics: Aged; Alleles; Ascorbic Acid; Body Mass Index; Cholesterol; Female; Follow-Up Studies; Fruit; Genotyping Techniques; Humans; Male; Mendelian Randomization Analysis; Middle Aged; Mortality; Myocardial Ischemia; Proportional Hazards Models; Risk Factors; Sensitivity and Specificity; Sodium-Coupled Vitamin C Transporters; Surveys and Questionnaires; Vegetables | 2015 |
Hypoglycemia in Non-diabetics During Development of Acute Coronary Ischemia.
The occurrence of hyperglycemia in non-diabetics during development of acute coronary ischemia (ACI) indicates latent glucose metabolism disorder, or is a case of newly discovered diabetes mellitus (DM) as a result of stress. Acute coronary syndrome refers to a group of clinical syndromes caused by a sudden circulatory disorder in coronary arteries, resulting in the corresponding myocardial ischemia. It covers range from unstable angina and myocardial infarction (MI) without Q wave in the electrocardiogram finding (NSTEMI) up to myocardial infarction with Q wave in the electrocardiogram finding (STEMI).. To determine the incidence of hyperglycemia in non-diabetics immediately after the occurrence of acute coronary ischemia and assess its risk factors.. The sample included 80 respondents. Men dominated with a total prevalence of 77.5%. The respondent was at mean age of 62.8±13.8 years. During the first measurement, immediately after hospital admission, 50% of respondents had increased blood glucose value and during the second measurement 62%. Hypertension as a risk factor has 54% and 56% smoking. The incidence of stress diabetes after ACI does not depend on the diagnosis of hypertension, χ(2)=0.050; p=0.823. The differences of mean values (median) BMI between examined persons with/without stress DM are not statistically significant p=0.402. Independent t-test showed that there was no statistically significant difference in the average values of HDL and LDL in patients with stress diabetes than in patients without diabetes stress after ACI p>0.05. For each year of age odds ratio for "stress diabetes" increases by 7% and 95% CI is 2% -12%.. The incidence of stress diabetes ACI is not dependent on the working diagnosis (MI or angina pectoris). As risk factors we set hypertension and current smoking. There were no statistically significant associations between active smoking and hypertension as a risk factor in relation to occurrence of stress diabetes. Topics: Acute Disease; Age Factors; Ascorbic Acid; Cholecalciferol; Dehydroepiandrosterone; Female; Humans; Hypertension; Hypoglycemia; Male; Middle Aged; Myocardial Ischemia; Nicotinic Acids; Plant Extracts; Risk Factors; Sex Factors | 2015 |
L-arginine attenuates oxidative stress condition during cardiomyopathy.
Increased production of oxygen free radicals and decreased oxidant capacity occur in coronary artery diseases (CAD) This pro-oxidant shift in intracellular redox state may induce cell death by either direct cell membrane damage by lipic peroxidation or apoptosis through activation of transcription factors. These changes occur not only in cardiomyocytes, bu also in cardiac sympathetic nerves, which are very sensitive to oxidative damage. Patients with heart failure encountel reduced peripheralblood flow at rest, during exercise and in response to endothelium-dependentvasodilators. Current treatments of cardiomyopathy, a degenerative condition of the myocardium frequently associated with heart failure have done little to enhance patient survival. Decreased myocardial contractility and altered regulation of peripheral circulation along with oxidative conditions are important contributors to the symptoms and prognosis of the disease process. Nitric oxide formed from L-arginine (2-amino-5 guanidinovaleric acid) metabolism in endothelial cells contributes to regulation of blood flow under these conditions. L-Arginine is the precursor of nitric oxide, an endogenous messenger molecule involved in a variety of endothelium-mediated physiological effects in the vascular system. In the present study, we investigated the effect of oral administration of L-arginine (3 g/day) on the intracellular redox status of the patients of ischemic cardiomyopathy aged 45-60 yrs. The enzymatic and non-enzymatic antioxidant parameters like superoxide dismutase, catalase, total thiols (TSH) and ascorbic acid along with pro-oxidant parameters, such as xanthine oxidase, as well as index of oxidative stress as protein carbonyl content and malondialdehyde (a marker of lipid peroxidation) were investigated in the plasma and RBC lysate. L-Arginine (3 g/day) administration was found to improve the levels of these parameters in the patients and regulate the blood flow, as evident by the improved blood pressure of the patients. Thus, it is inferred that L-arginine attenuates the oxidative stress conditions along with maintaining the blood pressure rate of patients suffering from cardiomyopathy. Topics: Antioxidants; Arginine; Ascorbic Acid; Cardiomyopathies; Catalase; Coronary Artery Disease; Female; Free Radicals; Humans; Male; Middle Aged; Models, Biological; Myocardial Ischemia; Oxidants; Oxidation-Reduction; Oxidative Stress; Reactive Oxygen Species; Superoxide Dismutase; Thyrotropin; Xanthine Oxidase | 2013 |
Post-ischaemic angiogenic therapy using in vivo prevascularized ascorbic acid-enriched myocardial artificial grafts improves heart function in a rat model.
Angiogenesis plays a key role in post-ischaemic myocardial repair. We hypothesized that epicardial implantation of an ascorbic acid (AA)-enriched myocardial artificial graft (MAG), which has been prevascularized in the recipients' own body, promotes restoration of the ischaemic heart. Gelatin patches were seeded with GFP-luciferase-expressing rat cardiomyoblasts and enriched with 5 μm AA. Grafts were prevascularized in vivo for 3 days, using a renal pouch model in rats. The MAG patch was then implanted into the same rat's ischaemic heart following myocardial infarction (MI). MAG-treated animals (MAG group, n = 6) were compared to untreated infarcted animals as injury controls (MI group, n = 6) and sham-operated rats as healthy controls (healthy group, n = 7). In vivo bioluminescence imaging indicated a decrease in donor cell survival by 83% during the first week post-implantation. Echocardiographic and haemodynamic assessment 4 weeks after MI revealed that MAG treatment attenuated left ventricular (LV) remodelling (LV end-systolic volume, 0.31 ± 0.13 vs 0.81 ± 0.01 ml, p < 0.05; LV end-diastolic volume 0.79 ± 0.33 vs 1.83 ± 0.26 ml, p < 0.076) and preserved LV wall thickness (0.21 ± 0.03 vs 0.09 ± 0.005 cm, p < 0.05) compared to the MI group. Cardiac output was higher in MAG than MI (51.59 ± 6.5 vs 25.06 ± 4.24 ml/min, p < 0.01) and comparable to healthy rats (47.08 ± 1.9 ml/min). Histology showed decreased fibrosis, and a seven-fold increase in blood vessel density in the scar area of MAG compared to MI group (15.3 ± 1.1 vs 2.1 ± 0.3 blood vessels/hpf, p < 0.0001). Implantation of AA-enriched prevascularized grafts enhanced vascularity in ischaemic rat hearts, attenuated LV remodelling and preserved LV function. Topics: Animals; Antigens; Ascorbic Acid; Cell Survival; Disease Models, Animal; Electrocardiography; Fibrosis; Heart Transplantation; Heart Ventricles; Hemodynamics; Male; Myocardial Ischemia; Myocardium; Neovascularization, Physiologic; Rats; Rats, Wistar; Ultrasonography; Ventricular Function, Left | 2013 |
[The experience of the application of ascorbinic acid as antioxidant after coronary artery surgery with use of cardiopulmonary bypass].
We have studied the role of oxidant stress in development of rhythm disturbances in early postoperative period after coronary artery bypass grafting and possibilities of their prevention with preparations of ascorbinic acid. It was shown that the use of β-adrenoblockers allows to prevent arrhythmia on first day after operation only in 80% of cases. Patients with developed disturbances of cardiac rhythm were characterized by high parameters of lipid peroxidation (LPO) and substantial changes of activity of antioxidant enzyme catalase. Administration of ascorbinic acid at the stage of preparation of patients to surgery and in first 24 hours after operation allowed to effectively prevent development of oxidative stress and disturbances of cardiac rhythm. A conclusion was made that inclusion of ascorbinic acid in drug therapy of patients with ischemic heart disease could be recommended for prevention of arrhythmia in postoperative period. Topics: Aged; Antioxidants; Arrhythmias, Cardiac; Ascorbic Acid; Coronary Artery Bypass; Drug Monitoring; Humans; Male; Middle Aged; Myocardial Ischemia; Oxidative Stress; Postoperative Care; Postoperative Complications; Time Factors; Treatment Outcome | 2012 |
Associations between dietary methods and biomarkers, and between fruits and vegetables and risk of ischaemic heart disease, in the EPIC Norfolk Cohort Study.
Methods for assessing diet are prone to measurement error, which may be substantial in large cohort investigations. Biomarkers can be used as objective measures with which to compare estimates of nutritional exposure using different methods. Cross sectional comparisons in 12 474 men and women of regression between biomarkers for vitamin C, sodium, potassium, fibre, carbohydrate, fat and phytoestrogens with intakes derived from food diaries and food frequency questionnaires (FFQ), and odds ratios for risk of ischaemic heart disease (IHD) by dietary and plasma vitamin C.. There were strong (P < 0.001) associations between biomarkers and intakes as assessed by food diary. Coefficients were markedly attenuated for data obtained from the FFQ, especially so for vitamin C, potassium and phytoestrogens (Z P < 0.05). Risk of IHD was associated with plasma vitamin C (P < 0.001) and intake of vitamin C and fruit and vegetables assessed by food diary (P quintile trends <0.001, 0.001) but not by the FFQ (P quintile trends 0.923, 0.186).. Nutritional data that reflect the findings from biomarkers reduce measurement error and will thus improve statistical power in studies of gene nutrient interactions in cohort studies. Topics: Aged; Ascorbic Acid; Biomarkers; Carotenoids; Cohort Studies; Diet; Diet Records; Diet Surveys; England; Female; Fruit; Humans; Male; Middle Aged; Myocardial Ischemia; Surveys and Questionnaires; Vegetables; Vitamins | 2008 |
Aminothiol redox alterations in patients with chronic heart failure of ischaemic or non-ischaemic origin.
Oxidative stress plays a role in the progression of chronic heart failure (CHF), but whether and how ischaemic heart disease (IHD) or non-IHD aetiology may account for differential redox alterations is currently unclear. We assessed the relation between thiol redox state and lipid peroxidation, as a marker of oxidative stress, in patients with CHF of ischaemic or non-ischaemic origin.. Blood reduced glutathione, plasma total and reduced cysteine, cysteinylglycine, homocysteine, glutathione, plasma alpha-tocopherol, ascorbic acid, and free malondialdehyde were assessed in 43 CHF heart transplant candidates (24 IHD and 19 non-IHD) and 30 controls matched for age, gender and number of atherosclerotic risk factors.. Reduced cysteine was increased in CHF patients compared with controls. The highest levels were found in IHD versus non-IHD patients versus controls. Malondialdehyde levels were significantly higher in IHD patients than in controls, whereas antioxidant vitamins did not differ among the three groups.. Specific abnormalities in the thiol pattern are associated with heart failure aetiology in CHF patients. Our findings point to the possible role of reduced cysteine in the progression of chronic IHD to heart failure status, as an additional pro-oxidant stimulus for worsening oxidative stress. Topics: Aged; alpha-Tocopherol; Ascorbic Acid; Biomarkers; Case-Control Studies; Chronic Disease; Cysteine; Dipeptides; Disease Progression; Female; Glutathione; Heart Failure; Homocysteine; Humans; Lipid Peroxidation; Male; Malondialdehyde; Middle Aged; Myocardial Ischemia; Oxidation-Reduction; Oxidative Stress; Research Design; Sulfhydryl Compounds | 2007 |
Adverse effects of free fatty acid associated with increased oxidative stress in postischemic isolated rat hearts.
The mechanisms of the adverse effects of free fatty acids on the ischemic-reperfused myocardium are not fully understood. Long-chain fatty acids, including palmitate, uncouple oxidative phosphorylation and should therefore promote the formation of oxygen-derived free radicals, with consequent adverse effects. Conversely, the antianginal agent trimetazidine (TMZ), known to inhibit cardiac fatty acid oxidation, could hypothetically lessen the formation of reactive oxygen species (ROS) and thus improve reperfusion mechanical function. Isolated perfused rat hearts underwent 30 min of total global ischemia followed by 30 min of reperfusion. Hearts were perfused with glucose 5.5 mmol/l or palmitate 1.5 mmol/l with or without TMZ (100 micromol/l). Ascorbyl free radical (AFR) release during perfusion periods was measured by electron spin resonance as a marker of oxidative stress. Post-ischemic recovery in the palmitate group of heart was lower than in the glucose group with a marked rise in diastolic tension and reduction in left ventricular developed pressure (Glucose: 85 +/- 11 mmHg; Palmitate: 10 +/- 6 mmHg; p < 0.001). TMZ decreased diastolic tension in both glucose- and in palmitate-perfused hearts. Release of AFR within the first minute of reperfusion was greater in palmitate-perfused hearts and in hearts perfused with either substrate, this marker of oxidative stress was decreased by TMZ (expressed in arbitrary units/ml; respectively: 8.49 +/- 1.24 vs. 1.06 +/- 0.70 p < 0.05; 12.47 +/- 2.49 vs. 3.37 +/- 1.29 p < 0.05). Palmitate increased the formation of ROS and reperfusion contracture. TMZ, a potential inhibitor of palmitate-induced mitochondrial uncoupling, decreased the formation of free radicals and improved postischemic mechanical dysfunction. The novel conclusion is that adverse effects of fatty acids on ischemic-reperfusion injury may be mediated, at least in part, by oxygen-derived free radicals. Topics: Animals; Ascorbic Acid; Fatty Acids, Nonesterified; Free Radicals; Heart; Male; Myocardial Contraction; Myocardial Ischemia; Myocardial Reperfusion Injury; Oxidation-Reduction; Oxidative Stress; Rats; Rats, Wistar; Trimetazidine; Vasodilator Agents | 2006 |
A newly synthesised molybdenum/ascorbic acid complex alleviates some effects of cardiomyopathy in streptozocin-induced diabetic rats.
Exogenous insulin does not prevent cardiac failure in patients with type 1 diabetes mellitus and a cardioprotective insulin mimic is greatly needed. Certain transition metals are known to act as insulin mimics and may be cardio- protective. In this study, the ability of a newly synthesised molybdenum/ascorbic acid complex to strengthen cardiac function was investigated.. Male CD rats were assigned to one of five groups: non-diabetic control, non-diabetic control treated with molybdenum/ascorbic acid complex, diabetic treated with sodium ascorbate, diabetic treated with molybdenum/ascorbic acid complex and untreated diabetics. Type 1 diabetes was induced by streptozocin injection. Once diabetes was confirmed, treatment was initiated by adding either the molybdenum/ascorbic acid complex or sodium ascorbate to the drinking water and continued for 6 weeks. Following the treatment period, the animals were terminated, and their hearts were excised and mounted in a working heart perfusion apparatus. Blood samples were taken for plasma glucose and plasma lipid level determination. Cardiac function was evaluated using 1 hour of low-flow ischaemic stress followed by 30 minutes of reperfusion.. Hearts from the animals treated with the molybdenum/ascorbic acid complex displayed the best aerobic performance of all the diabetic animals. Blood glucose levels and blood lipid levels were significantly lower in animals treated with the complex than in other diabetic animals. The group treated with the complex also had a lower drinking rate than the other diabetic groups. Furthermore, hearts from animals treated with the molybdenum/ascorbic acid complex showed a greater degree of recovery from low-flow ischaemia than any other group.. The molybdenum/ascorbic acid complex showed some significant insulin-mimic and cardioprotective effects. Further development of this complex could provide a drug useful for alleviating some of the cardiovascular problems associated with diabetes mellitus. Topics: Animals; Ascorbic Acid; Blood Glucose; Cardiomyopathies; Diabetes Mellitus, Experimental; Heart; Insulin; Lipids; Male; Molybdenum; Myocardial Ischemia; Rats; Rats, Inbred Strains; Streptozocin | 2006 |
Consensus meeting on "Relevance of parenteral vitamin C in acute endothelial dependent pathophysiological conditions (EDPC)".
The 22 supersetnd Hohenheim Consensus Workshop took place in at the University of Stuttgart-Hohenheim. The subject of this conference was vitamin C and its role in the treatment of endothelial dysfunction. Scientists, who had published and reviewed scientific and regulatory papers on that topic were invited, among them basic researchers, toxicologists, clinicians and nutritionists. The participants were presented with eleven questions, which were discussed and answered at the workshop, with the aim of summarising the current state of knowledge. The explicatory text accompanying the short answers was produced and agreed on after the conference and was backed up by corresponding references. The therapeutic relevance of administration of the physiological antioxidant vitamin C in high parenteral doses in Endothelial Dependent Pathophysiological Conditions (EDPC) was discussed. Endothelial dysfunction is defined as including disturbed endothelial dependant relaxation of resistance vessels, breakdown of the microvascular endothelial barrier and/or loss of anti-adhesive function. It occurs in severe burn injury, intoxications, acute hyperglycemia, sepsis, trauma, and ischemic-reperfusion tissue injury and is induced by oxidative stress. Reduced plasma ascorbate levels are a hallmark of oxidative stress and occur in severe burns, sepsis, severe trauma, intoxication, chemotherapy/radiotherapy and organ transplantation. Vitamin C directly enhances the activity of nitric oxide synthase, the acyl CoA oxidase system and inhibits the actions of proinflammatory lipids. There is experimental evidence that parenteral high-dose vitamin C restores endothelial function in sepsis. In vitro, supraphysiological concentrations (> 1mM) of ascorbate restore nitric oxide bioavailability and endothelial function. Only parenterally, can enough vitamin C be administered to combat oxidative stress. There is no evidence that parenteral vitamin C exerts prooxidant effects in humans. Theoretical concerns in relation to competitive interactions between vitamin C and glucose cellular uptake are probably only relevant for oxidised vitamin C (dehydroascorbate). Topics: Acute Disease; Acyl-CoA Oxidase; Ascorbic Acid; Burns; Endothelium, Vascular; Glucose; Heart Failure; Humans; Hyperglycemia; Infusions, Parenteral; Myocardial Ischemia; Nitric Oxide Synthase Type III; Oxidative Stress; Poisoning; Reperfusion Injury; Sepsis | 2006 |
Antioxidant intervention attenuates myocardial neovascularization in hypercholesterolemia.
Hypercholesterolemia (HC) and atherosclerosis can elicit oxidative stress, coronary endothelial dysfunction, and myocardial ischemia, which may induce growth-factor expression and lead to myocardial neovascularization. We tested the hypothesis that chronic antioxidant intervention in HC would attenuate neovascularization and preserve the expression of hypoxia-inducible factor (HIF)-1alpha and vascular endothelial growth factor (VEGF).. Three groups of pigs (n=6 each) were studied after 12 weeks of normal or 2% HC diet or HC+antioxidant supplementation (100 IU/kg vitamin E and 1 g vitamin C daily). Myocardial samples were scanned ex vivo with a novel 3D micro-CT scanner, and the spatial density and tortuosity of myocardial microvessels were determined in situ. VEGF mRNA, protein levels of VEGF and VEGF receptor-1, HIF-1alpha, nitrotyrosine, and superoxide dismutase (SOD) were determined in myocardial tissue. The HC and HC+antioxidant groups had similar increases in serum cholesterol levels. HC animals showed an increase in subendocardial spatial density of microvessels compared with normal (160.5+/-11.8 versus 95.3+/-8.2 vessels/cm2, P<0.05), which was normalized in HC+antioxidant (92.5+/-20.5 vessels/cm2, P<0.05 versus HC), as was arteriolar tortuosity. In addition, HC induced upregulation of VEGF, HIF-1alpha, and nitrotyrosine expression and decreased SOD expression and activity, all of which were preserved by antioxidant intervention.. Changes in myocardial microvascular architecture invoked by HC are accompanied by increases in HIF-1alpha and VEGF expression and attenuated by antioxidant intervention. This underscores a role of increased oxidative stress in modulating myocardial microvascular architecture in early atherogenesis. Topics: Animals; Antioxidants; Arteriosclerosis; Ascorbic Acid; Cardiotonic Agents; Coronary Circulation; Diet, Atherogenic; Dinoprost; Enzyme Induction; Female; Gene Expression Profiling; Gene Expression Regulation; Heart; Hypercholesterolemia; Hypoxia-Inducible Factor 1, alpha Subunit; Imaging, Three-Dimensional; Myocardial Ischemia; Neovascularization, Pathologic; Oxidative Stress; Superoxide Dismutase; Swine; Tomography, X-Ray Computed; Transcription Factors; Tyrosine; Vascular Endothelial Growth Factor A; Vitamin E | 2004 |
Vitamin C deficiency exerts paradoxical cardiovascular effects in osteogenic disorder Shionogi (ODS) rats.
Vitamin C is considered to be a very efficient water-soluble antioxidant, for which several new cardiovascular properties were recently described. The aim of this study was to determine in vivo the effects of a severe depletion of vitamin C on cardiac and vascular variables and reperfusion arrhythmias. For this purpose, we used a mutant strain of Wistar rats, osteogenic disorder Shionogi (ODS). After 15 d of consuming a vitamin C-deficient diet, ODS rats had a 90% decrease in plasma and tissue levels of ascorbate compared with ODS vitamin C-supplemented rats and normal Wistar rats. However, plasma antioxidant capacity, proteins, alpha-tocopherol, urate, catecholamines, lipids, and nitrate were not influenced by the vitamin C deficiency in ODS rats. Moreover, there was no difference between ODS vitamin C-deficient and -supplemented rats in heart rate and arterial pressure. After 5 min of an in vivo regional myocardial ischemia, various severe arrhythmias were observed, but their intensities were not modified by vitamin C in vitamin C-deficient ODS rats. The vascular reactivity, measured in vitro on thoracic arteries, was not altered by ascorbate deficiency in ODS rats. These unexpected results suggest that unidentified compensatory mechanisms play a role in maintaining normal cardiac function and vascular reactivity in vitamin C-deficient rats. Topics: Acetylcholine; alpha-Tocopherol; Animals; Aorta; Arrhythmias, Cardiac; Ascorbic Acid; Ascorbic Acid Deficiency; Blood Pressure; Bone Diseases; Cardiovascular Diseases; Diet; Epinephrine; Heart Rate; Male; Muscle Contraction; Myocardial Ischemia; Myocardial Reperfusion; Norepinephrine; Osteogenesis; Phenylephrine; Rats; Rats, Mutant Strains; Rats, Wistar | 2004 |
Vitamin C inhibits hypoxia-induced damage and apoptotic signaling pathways in cardiomyocytes and ischemic hearts.
Reactive oxygen species play a central role in myocardial ischemic injury and are a target for therapeutic intervention. Vitamin C is an essential antioxidant yet difficult to deliver in pharmacologic concentration to the myocardium. We found that adult rat cardiomyocytes accumulate vitamin C by transporting dehydroascorbic acid (DHA), the oxidized form of vitamin C, but do not transport ascorbic acid. Loading cells with vitamin C by DHA treatment resulted in resistance to hypoxia- and hypoxia/reoxygenation-induced cell death associated with the quenching of reactive oxygen species. When rats were injected with DHA before coronary occlusion, the ascorbic acid content in the heart was six to eight times higher than in untreated controls and myocardial infarction was reduced by 62%. DHA also provided significant protection when administered intravenously 2 h after coronary occlusion. In cardiomyocytes subjected to hypoxia/reoxygenation, DHA treatment resulted in decreased apoptosis associated with inhibition of Bax expression, caspase-3 activation, and cytochrome c translocation into the cytoplasm. DHA treatment also inhibited Jak2, STAT1, and STAT5 phosphorylation, and increased STAT3 phosphorylation, in hypoxic cardiomyocytes and ischemic myocardial tissue. Our findings suggest that DHA may be useful as a cardioprotectant in ischemic heart disease. Topics: Animals; Apoptosis; Ascorbic Acid; Cell Hypoxia; Dehydroascorbic Acid; Disease Models, Animal; Heart; Hypoxia; Muscle Cells; Myocardial Ischemia; Myocardium; Rats; Rats, Sprague-Dawley; Signal Transduction | 2004 |
Pyruvate improves mitochondrial bioenergetics in an ex-vivo animal model of myocardial ischemia.
Pyruvate is an energy substrate with known cardioprotective activity. We know now that this is due not only to its antioxidant activity, but also to its reduction of intracellular acidosis, modulation of intracytosolic calcium and improvement of cardiomyocyte contractility. However, the role of cardiac mitochondria in such positive effects has only recently begun to be understood and the exact mechanisms of the effect of pyruvate on mitochondria are still largely unknown. Aiming to study the effect of pyruvate on cardiac mitochondrial function during acute ischemia, we used an ex-vivo animal model, perfused in a Langendorff system and then subjected to ischemia in the presence and absence of pyruvate. We evaluated the mitochondrial membrane electrical potential, the respiratory chain O2 consumption (and respiratory control ratio) and the energy charges generated with different energy substrates. We conclude that pyruvate has some effect on the mitochondrial oxidative system (by non-significantly improving the respiratory control ratio), but its main action is on the phosphorylation system, significantly decreasing the time taken to complete a phosphorylation cycle (lag phase) and improving ATP production (increase in energy charge), thus allowing better maintenance of mitochondrial membrane structure, with consequent improvement of the electrical potential after a phosphorylation cycle. These findings have enabled better understanding of the mechanisms behind pyruvate cytoprotection in ischemic cardiomyopathy, clearly highlighting the essential role of cardiac mitochondria in this process. Topics: Animals; Ascorbic Acid; Chemotherapy, Cancer, Regional Perfusion; Female; Glutamic Acid; Intracellular Membranes; Malates; Male; Membrane Potentials; Mitochondria, Heart; Models, Animal; Myocardial Ischemia; Oxidoreductases, N-Demethylating; Oxygen Consumption; Phosphorylation; Pyruvic Acid; Rats; Rats, Wistar; Succinic Acid | 2003 |
Cardioprotective and antioxidant effects of apomorphine.
Apomorphine is a potent antioxidant that infiltrates through biological membranes. We studied the effect of apomorphine (2 microM) on myocardial ischemic-reperfusion injury in the isolated rat heart. Since iron and copper ions (mediators in formation of oxygen-derived free radicals) are released during myocardial reperfusion, apomorphine interaction with iron and copper and its ability to prevent copper-induced ascorbate oxidation were studied. Apomorphine perfused before ischemia or at the commencement of reperfusion demonstrated enhanced restoration of hemodynamic function (i.e. recovery of the work index (LVDP x HR) was 69.2 +/- 4.0% with apomorphine pre-ischemic regimen vs. 43.4 +/- 9.01% in control hearts, p < 0.01, and 76.3 +/- 8.0% with apomorphine reperfusion regimen vs. 30.4 +/- 11.1% in controls, p < 0.001). This was accompanied by decreased release of proteins in the effluent and improved coronary flow recovery in hearts treated with apomorphine after the ischemia. Apomorphine forms stable complexes with copper and with iron, and inhibits the copper-induced ascorbate oxidation. It is suggested that these iron and copper chelating properties and the redox-inactive chelates formed by transition metals and apomorphine play an essential role in post-ischemic cardioprotection. Topics: Animals; Antioxidants; Apomorphine; Ascorbic Acid; Copper; Coronary Circulation; Dopamine Agonists; Dose-Response Relationship, Drug; Free Radicals; Heart; Ions; Iron; Male; Models, Chemical; Myocardial Ischemia; Myocardial Reperfusion; Myocardial Reperfusion Injury; Myocardium; Oxidation-Reduction; Oxygen; Rats; Rats, Sprague-Dawley; Spectrophotometry; Time Factors | 2003 |
Vitamin C intake and risk of ischemic heart disease in a population with a high prevalence of smoking.
Epidemiological data on the relationship between vitamin C intake and ischemic heart disease (IHD) risk are limited in the Asian population, with a high prevalence of smoking. This study aims to investigate the association between vitamin C intake and the incidence of non-fatal IHD in Korean men.. The case group consisted of 108 patients with electrocardiogram-confirmed myocardial infarction or angiographically confirmed (>or=50% stenosis) coronary artery disease (CAD) who were admitted to a university teaching hospital in Seoul, Korea. The controls were 142 age-matched patients admitted to the departments of ophthalmology and orthopedic surgery at the same hospital. Vitamin C intake was assessed by a nutritionist using a semi-quantitative food frequency method, and body mass index (BMI), tobacco use and past history of cardiovascular disease were determined by examination and interview.. After controlling for cardiovascular risk factors, including BMI, smoking, past history of hypertension, past history of hyperlipidemia, dietary intakes of energy, total fat (or subtype of fat), cholesterol, beta-carotene, and vitamin E, the odds ratio (OR) of non-fatal IHD was 0.34 (95% confidence interval (CI) 0.13-0.90) in the highest tertile of vitamin C intake compared with those in the lowest tertile. In a subgroup analysis, which compared nonsmokers in the highest tertile of vitamin C intake to current smokers in the lowest tertile of vitamin C intake, the odds ratio of developing non-fatal IHD was 0.12 (95% CI 0.02-0.77).. This study suggests that higher intake of vitamin C is associated with the decreased risk of non-fatal IHD in a population with a high prevalence of smoking. Topics: Antioxidants; Ascorbic Acid; Case-Control Studies; Confidence Intervals; Feeding Behavior; Humans; Korea; Male; Middle Aged; Multivariate Analysis; Myocardial Infarction; Myocardial Ischemia; Odds Ratio; Prevalence; Risk Factors; Smoking; Surveys and Questionnaires | 2003 |
Relation between plasma ascorbic acid and mortality in men and women in EPIC-Norfolk prospective study: a prospective population study. European Prospective Investigation into Cancer and Nutrition.
Ascorbic acid (vitamin C) might be protective for several chronic diseases. However, findings from prospective studies that relate ascorbic acid to cardiovascular disease or cancer are not consistent. We aimed to assess the relation between plasma ascorbic acid and subsequent mortality due to all causes, cardiovascular disease, ischaemic heart disease, and cancer.. We prospectively examined for 4 years the relation between plasma ascorbic acid concentrations and mortality due to all causes, and to cardiovascular disease, ischaemic heart disease, and cancer in 19 496 men and women aged 45-79 years. We recruited individuals by post using age-sex registers of general practices. Participants completed a health and lifestyle questionnaire and were examined at a clinic visit. They were followed-up for causes of death for about 4 years. Individuals were divided into sex-specific quintiles of plasma ascorbic acid. We used the Cox proportional hazard model to determine the effect of ascorbic acid and other risk factors on mortality.. Plasma ascorbic acid concentration was inversely related to mortality from all-causes, and from cardiovascular disease, and ischaemic heart disease in men and women. Risk of mortality in the top ascorbic acid quintile was about half the risk in the lowest quintile (p<0.0001). The relation with mortality was continuous through the whole distribution of ascorbic acid concentrations. 20 micromol/L rise in plasma ascorbic acid concentration, equivalent to about 50 g per day increase in fruit and vegetable intake, was associated with about a 20% reduction in risk of all-cause mortality (p<0.0001), independent of age, systolic blood pressure, blood cholesterol, cigarette smoking habit, diabetes, and supplement use. Ascorbic acid was inversely related to cancer mortality in men but not women.. Small increases in fruit and vegetable intake of about one serving daily has encouraging prospects for possible prevention of disease. Topics: Age Distribution; Aged; Ascorbic Acid; Cardiovascular Diseases; Cause of Death; Female; Humans; Male; Middle Aged; Myocardial Ischemia; Neoplasms; Proportional Hazards Models; Prospective Studies; Registries; Risk Factors; Sex Distribution; Surveys and Questionnaires | 2001 |
[Effects of biologically active supplements on the antioxidant and vitamin status of patients with hypertension and ischemic heart disease].
Biologically active additives in integrated therapy of patients with cardiovascular diseases against a background body overweight. The influence of antiaterosclerotic diet with including some biologically active additives, which contain vitamins C, E, B2, B6, beta-carotene, Zn, Mg, Na, K, Ca, I was studied in 91 patients with ischemic heart disease, hypertension disease. The usage of biologically active additives during 4 weeks has promoted positive changes of clinical symptoms of diseases against a background of lowering of serum cholesterol, triglycerides and increasing of vitamins A, E, C, B2, B6. Topics: Adult; Antioxidants; Ascorbic Acid; beta Carotene; Blood Glucose; Cholesterol; Dietary Supplements; Humans; Hypertension; Lipid Peroxidation; Middle Aged; Myocardial Ischemia; Pyridoxine; Riboflavin; Time Factors; Triglycerides; Vitamin E; Vitamins | 2001 |
Exposure to environmental tobacco smoke is associated with lower plasma beta-carotene levels among nonsmoking women married to a smoker.
We evaluated the association between exposure to environmental tobacco smoke (ETS) from husbands who smoke and plasma levels of antioxidant vitamins among nonsmoking women. A total of 1249 women from four areas in Italy answered a self-administered questionnaire, reported their diets on a food frequency questionnaire, had a medical examination, and gave their blood for alpha and beta-carotene, retinol, L-ascorbic acid, alpha-tocopherol, and lycopene determinations. Urinary cotinine was used to evaluate the level of recent exposure to ETS. After adjusting for study center, age and education, we found no association between ETS exposure and daily nutrient intake of beta-carotene, retinol, L-ascorbic acid, and alpha-tocopherol. However, we found an inverse dose-response relationship between intensity of current husband's smoke and concentrations of plasma beta-carotene and L-ascorbic acid. The associations remained even after controlling for daily beta-carotene and vitamin C intake and for other potential confounders (vitamin supplementation, alcohol consumption, and body mass index). Moreover, when urinary cotinine was considered as the exposure variable, a significant inverse association with plasma beta-carotene was found. The findings may be of interest to explain the biological mechanism that link ETS exposure with lung cancer and ischemic heart diseases. Topics: Adult; Aged; Ascorbic Acid; beta Carotene; Cross-Sectional Studies; Environmental Exposure; Female; Humans; Lung Neoplasms; Male; Middle Aged; Myocardial Ischemia; Spouses; Tobacco Smoke Pollution | 2001 |
Effects of dietary polyunsaturated fatty acids and hepatic steatosis on the functioning of isolated working rat heart under normoxic conditions and during post-ischemic reperfusion.
The purpose of this study was to modify the amount of 22:4 n-6, 22:5 n-6 and 20:5 n-3 in cardiac phospholipids and to evaluate the influence of these changes on the functioning of working rat hearts and mitochondrial energy metabolism under normoxic conditions and during postischemic reperfusion. The animals were fed one of these four diets: (i) 10% sunflower seed oil (SSO); (ii) 10% SSO + 1% cholesterol; (iii) 5% fish oil (FO, EPAX 3000TG, Pronova) + 5% SSO; (iv) 5% FO + 5% SSO + 1% cholesterol. Feeding n-3 PUFA decreased n-6 PUFA and increased n-3 PUFA in plasma lipids. In the phospholipids of cardiac mitochondria, this dietary modification also induced a decrease in the n-6/n-3 PUFA ratio. Cholesterol feeding induced marked hepatic steatosis (HS) characterized by the whitish appearance of the liver. It also brought about marked changes in the fatty acid composition of plasma and mitochondrial phospholipids. These changes, characterized by the impairment of deltaS- and delta6-desaturases, were more obvious in the SSO-fed rats, probably because of the presence of the precursor of the n-6 family (linoleate) in the diet whereas the FO diet contained large amounts of eicosapentaenoic and docosahexaenoic acids. In the mitochondrial phospholipids of SSO-fed rats, the (22:4 n-6 + 22:5 n-6) to 18:2 n-6 ratio was decreased by HS, without modification of the proportion of 20:4 n-6. In the mitochondrial phospholipids of FO-fed rats, the amount of 20:5 n-3 tended to be higher (+56%). Cardiac functioning was modulated by the diets. Myocardial coronary flow was enhanced by HS in the SSO-fed rats, whereas it was decreased in the FO-fed animals. The rate constant k012 representing the activity of the adenylate kinase varied in the opposite direction, suggesting that decreased ADP concentrations could cause oxygen wasting through the opening of the permeability transition pore. The recovery of the pump function tended to be increased by n-3 PUFA feeding (+22%) and HS (+45%). However, the release of ascorbyl free radical during reperfusion was not significantly modified by the diets. Conversely, energy production was increased by ischemia/reperfusion in the SSO group, whereas it was not modified in the FO group. This supports greater ischemia/reperfusion-induced calcium accumulation in the SSO groups than in the FO groups. HS did not modify the mitochondrial energy metabolism during ischemia/reperfusion. Taken together, these data suggest that HS- and n-3 PUFA-induced de Topics: Adenine; Animals; Aorta; Ascorbic Acid; Body Weight; Cardiac Output; Cell Respiration; Cholesterol, Dietary; Coronary Circulation; Dietary Fats; Fatty Acids, Unsaturated; Fish Oils; Free Radicals; Heart; Liver; Mitochondria, Heart; Myocardial Ischemia; Organ Size; Oxygen; Palmitoylcarnitine; Phosphates; Plant Oils; Pyruvic Acid; Rats; Reperfusion Injury; Sunflower Oil | 2001 |
[Biologically active food supplements in comprehensive therapy of patients with ischemic heart disease and hypertension and the background of overweight].
The influence of anti-atherosclerotic diet with including some biologically active additives, with contain vitamins C, E, beta-carotene, Zn, Cr, Se was studied in 80 patients with ischemic heart disease, hypertension disease. The usage of biologically active additives during 4 weeks has promoted positive changes of clinical symptoms of diseases against a background of lowering of serum cholesterol, triglycerides and increasing of IgA, IgG, vitamins A, E, C. Topics: Adult; Ascorbic Acid; Cholesterol; Chromium; Complement C3; Diet, Reducing; Female; Humans; Hypertension; Immunoglobulins; Male; Middle Aged; Minerals; Myocardial Ischemia; Obesity; Selenium; Triglycerides; Vitamin E; Vitamins; Zinc | 2000 |
Effect of deferoxamine on post-hypoxic-ischemic reperfusion injury of the newborn lamb heart.
Post-hypoxic-ischemic (HI) reperfusion induces excess production of non-protein-bound iron (NPBI), leading to formation of the highly reactive hydroxyl radical. We investigated whether the iron-chelator deferoxamine (DFO) could reduce reperfusion injury and improve left ventricular (LV) function. We produced severe HI in 14 newborn lambs and measured pre-HI, upon reperfusion, 60 and 120 min after HI the following parameters: mean aortic blood pressure, total peripheral resistance, stroke volume (SV), ejection fraction (EF) and LV contractility (pre-HI, 60 and 120 min post-HI). These parameters were assessed by measuring LV pressure (tip manometer) and volume (conductance catheter), using inflow occlusion to obtain slope (Ees) and volume intercept of the end-systolic P-V relationship (V10). We determined the antioxidative capacity, i.e. the ratio of ascorbic acid and dehydroascorbic acid (AA/DHAA) and malondialdehyde from coronary sinus blood at pre-HI and at 15, 60 and 120 min post-HI. Seven lambs received DFO (10 mg/kg i.v.) immediately after HI, 6 control lambs received a placebo. While neither Ees nor EF changed significantly in either group, the volume intercept V10 in the DFO-treated group was significantly smaller (0.25 +/- 0.03 vs. 0.70 +/- 0.09, p < 0.05), whereas SV was larger (3.6 +/- 0.6 vs. 2.2 +/- 0.2 ml, p < 0.05) and the AA/DHAA ratio was significantly lower at 15 min post-HI (p < 0.05) providing evidence for HI damage and for the protective effect of DFO.. post-HI treatment of the newborn lamb with DFO has a modifying effect on free radical-induced damage to the myocardium and protects myocardial performance. Topics: Animals; Animals, Newborn; Ascorbic Acid; Chelating Agents; Deferoxamine; Dehydroascorbic Acid; Female; Heart; Hypoxia; Male; Malondialdehyde; Myocardial Ischemia; Myocardial Reperfusion Injury; Myocardium; Oxidation-Reduction; Sheep | 1999 |
Influence of the severity of myocardial ischemia on the intensity of ascorbyl free radical release and on postischemic recovery during reperfusion.
Ascorbyl free radical (AFR), can be considered as an atoxic and endogenous indicator of oxidative stress. The purpose of our experiments was to investigate the influence of the severity and length of ischemia on the extent of AFR release during myocardial ischemia and reperfusion. For that purpose, isolated perfused rat hearts were submitted to a global ischemia, either total (residual flow 0%) or low flow (residual flow 5%), of 20 or 60 min length. Coronary effluents were collected at different times of experimentation and analyzed with Electron Spin Resonance (ESR) spectroscopy. AFR ESR doublet (g = 2.0054, aH = 0.188 MT) was not detected in coronary effluents collected during control perfusion periods. Nevertheless, during low-flow ischemia, a weak AFR release was noted. Moreover, a sudden and massive AFR liberation was observed at the time of reperfusion: this AFR release was weaker after low-flow ischemia than after total ischemia and was enhanced when the duration of ischemia increased from 20 min to 60 min. The large liberation of AFR noticed during global total ischemia was associated with a greater depression in myocardial contractile function and a lower recovery in coronary flow. In conclusion, our study demonstrates that AFR production at the time of reperfusion depends on the duration and strength of the ischemia, and is related to free radical injury. According to previously described ascorbate/AFR properties, we can conclude that AFR liberation in coronary effluents could represent a marker of oxidative stress during ischemia and/or reperfusion of hearts. This AFR release could be considered a sign of the severity of the ischemic episode, and could be related to the functional impairment during reperfusion. Topics: Animals; Ascorbic Acid; Blood Pressure; Coronary Circulation; Coronary Vessels; Dehydroascorbic Acid; Electron Spin Resonance Spectroscopy; Free Radicals; Heart Rate; Male; Myocardial Ischemia; Myocardial Reperfusion; Myocardium; Oxidative Stress; Rats; Rats, Wistar; Ventricular Function, Left | 1998 |
Electron spin resonance measure of brain antioxidant activity during ischemia/reperfusion.
An electron spin resonance technique was used to measure cerebral antioxidant activity during asphyxial cardiac arrest and reperfusion. There were significant decreases in ascorbate (48%), glutathione (44%), total thiols (42%), protein thiols (38%) and alpha-tocopherol (26%) in the hippocampus 10 min after reperfusion (p < 0.05 vs respective baselines) but not during asphyxial cardiac arrest. The levels of antioxidants returned to baseline values by 120 min after reperfusion. The results support the hypothesis that reperfusion from asphyxial cardiac arrest, but not arrest alone, produced a significant oxidative stress as reflected by a depletion of both water and lipid soluble antioxidants. Furthermore, antioxidant depletion was transient, with normal antioxidant levels observed 120 min, 24 h and 72 h after reperfusion. Topics: Analysis of Variance; Animals; Antioxidants; Ascorbic Acid; Asphyxia; Carbon Dioxide; Consciousness; Cranial Nerves; Electron Spin Resonance Spectroscopy; Glutathione; Heart Arrest; Hippocampus; Monophenol Monooxygenase; Myocardial Ischemia; Myocardial Reperfusion; Nerve Tissue Proteins; Oxidative Stress; Oxygen; Partial Pressure; Rats; Rats, Sprague-Dawley; Respiration; Sulfhydryl Compounds; Time Factors; Vitamin E | 1998 |
Networking antioxidants in the isolated rat heart are selectively depleted by ischemia-reperfusion.
Although cardiac endogenous antioxidants have been reported to be oxidized and decreased by ischemia-reperfusion, little is known whether the changes in these antioxidants are correlated with each other in a systematic relationship. In this study, isolated rat hearts were subjected to various periods of ischemia-reperfusion using the Langendorff method, and the content and/or redox status of tissue antioxidants were analyzed. Significant losses in the tissue hydrophilic antioxidants, ascorbate, and glutathione were observed. These losses were dependent on the duration of the reperfusion period (between 0-40 min) but not of ischemia (20-60 min). Marked increases of dehydroascorbate and glutathione disulfide, the oxidized forms of ascorbate and glutathione, respectively, were found during reperfusion, but these changes were not observed during ischemia. These findings indicate that the tissue hydrophilic antioxidants are easily oxidized and may be the first line of antioxidant defenses during reperfusion. Lipophilic antioxidants, like ubiquinol 9 and vitamin E, were not decreased during ischemia-reperfusion using regular buffer; however, if oxidative stress was induced by addition of H2O2 to the buffer solution during reperfusion after 20 min of ischemia, decreases in both the hydrophilic and hydrophobic antioxidants were noticeable. With 100 microM H2O2, the tissue antioxidant decreases were ubiquinol 9 (39%), vitamin E (3%), glutathione (44%) and ascorbate (58%). Only with 500 microM H2O2 treatment were marked decreases in tissue vitamin E (65%) observed; this was associated with almost complete depletion of tissue ubiquinol 9 (95%). These results suggest that prior to the consumption of vitamin E, other antioxidants are depleted and that vitamin E may serve as the ultimate antioxidant, protecting the integrity of cellular membranes. Thus, in this work, cardiac antioxidants were demonstrated to change in a systematically organized relationship under ischemia-reperfusion. This graded utilization of antioxidants supports the redox based antioxidant network concept, found to be present in other biological systems. Topics: Animals; Antioxidants; Ascorbic Acid; Dehydroascorbic Acid; Glutathione; Glutathione Disulfide; Hydrogen Peroxide; In Vitro Techniques; Male; Myocardial Ischemia; Myocardial Reperfusion; Rats; Rats, Sprague-Dawley; Ubiquinone; Vitamin E | 1998 |
Plasminogen activator inhibitor-1, the acute phase response and vitamin C.
Epidemiologial studies suggest that elevated plasma plasminogen activator inhibitor-1 (PAI-1) activity is associated with ischaemic heart disease. Based on our earlier work suggesting a link between plasma fibrinogen, infection and low vitamin C status, we sought to determine whether similar relationships existed for PAI-1 activity. We performed a longitudinal study of cardiovascular disease risk factors in 96 volunteers aged 65-74 years, living in the community in Cambridge. Each subject was visited at home 7 times over a 14 month period. Plasma PAI-1 activity, serum ascorbate, markers of the acute phase response, serum lipids and other cardiovascular disease risk factors were measured on each occasion. In a multiple regression analysis, the three significant predictors of PAI-1 activity were body mass index (P = 0.0001), blood neutrophil count (P = 0.03) and, inversely, serum ascorbate (P = 0.003). The inverse relationship between PAI-1 activity and serum ascorbate persisted even when vitamin C supplement takers or smokers were excluded from the analysis. Serum ascorbate was strongly related to estimated dietary intake of vitamin C (P < 0.0001). Low serum ascorbate is associated with high PAI-1 activity which is, in turn, associated with increased ischaemic heart disease risk. We hypothesise that activation of the acute phase response by infection could increase PAI-1 activity and, consequently, also increase the risk of coronary artery thrombosis. Furthermore, we suggest that vitamin C could attenuate this response. Topics: Acute-Phase Reaction; Aged; Ascorbic Acid; Female; Fibrinogen; Humans; Male; Middle Aged; Myocardial Ischemia; Plasminogen Activator Inhibitor 1; Risk Factors; Seasons | 1997 |
Dietary iron alters liver, erythrocyte and plasma antioxidant and nitrite levels, and also sensitizes the heart to ischemia/reperfusion.
The aim of the study was to determine whether dietary iron within the normal range is (i) responsible for oxidative changes in the liver, erythrocytes and plasma; and (ii) make the heart more susceptible to ischemia/reperfusion injury. Female rats were allocated to four groups according to diet supplemented with either 15, 35, 150, or 300 mg iron/kg diet. After 4 months the following statistical difference in the two higher dietary groups were observed compared to the lower ones: (i) decreased antioxidant concentrations in liver, plasma and erythrocytes (alpha-tocopherol and ascorbic acid); (ii) increased plasma nitrite concentration; (iii) ischemia/reperfusion elevated LMWI and MDA concentrations and decreased ascorbate concentrations. This study clearly showed that increased dietary iron concentration causes oxidative changes in plasma, erythrocytes and liver. Higher dietary iron aggravated the outcome of ischemia/reperfusion injury as indicated by an elevated malondialdehyde concentration in the two higher dietary iron groups. Topics: Animals; Antioxidants; Ascorbic Acid; Catalase; Erythrocytes; Female; Glutathione Peroxidase; Heart; Iron; Iron, Dietary; Liver; Malondialdehyde; Mitochondria, Liver; Myocardial Ischemia; Myocardial Reperfusion Injury; Myocardium; Nitrates; Nitric Oxide; Nitrites; Oxidation-Reduction; Rats; Rats, Sprague-Dawley; Superoxide Dismutase; Vitamin E | 1997 |
In vivo, continuous and automatic monitoring of extracellular ascorbic acid by microdialysis and on-line liquid chromatography.
A system for in vivo, automatic, continuous monitoring of organ extracellular ascorbic acid in anesthetized rat is described. This system involves microdialysis perfusion and a LC system equipped with an electrochemical detector. Microdialysate, eluted from a microdialysis probe implanted in the brain cortex or in the left ventricular myocardium of anesthetized rats was collected in the sample loop of an on-line injector for direct injection onto the LC system. This automated method provides a shortened sample processing time. This system was utilized to investigate the effect of cerebral ischemia on cortex extracellular ascorbic acid and the effect of myocardial ischemia on left ventricular myocardium extracellular ascorbic acid in anesthetized rats. Basal ascorbic acid concentrations in the cortex and left ventricular myocardium ranged from 9.7 to 15.4 microM (mean +/- S.D., 12.7 +/- 2.5 microM from the results of eight rats) and from 9.3 to 36.0 microM (mean +/- S.D., 24.3 +/- 8.9 microM from the results of twelve rats), respectively. Cerebral ischemia significantly elevated ascorbic acid levels in the cortex extracellular space, while myocardial ischemia did not significantly alter ascorbic acid levels in the left ventricular myocardium extracellular space. Topics: Animals; Ascorbic Acid; Brain Ischemia; Cerebral Cortex; Chromatography, Liquid; Extracellular Space; Female; Heart Ventricles; Male; Microdialysis; Myocardial Ischemia; Rats; Rats, Sprague-Dawley | 1996 |
Role of ascorbate in protection by nitecapone against cardiac ischemia-reperfusion injury.
The antioxidant properties of nitecapone, a catechol derivative and an inhibitor of catechol-O-methyltransferase, were reported recently. In the present study, the influence of nitecapone on isolated rat heart ischemia-reperfusion injury was investigated to elucidate its cardioprotective role. Nitecapone, administered in the perfusion buffer from the beginning of the pre-ischemic phase, significantly improved recovery of cardiac mechanical function, suppressed enzyme leakage in the coronary effluent, and minimized loss of ascorbate, compared with the control group. In rats fed a diet containing 4% ascorbate, myocardial ascorbate content in ascorbate-fed rats after ischemia-reperfusion was higher than that in control rats fed a normal diet without ischemia. However, supplemented rats did not show any beneficial effects on cardiac mechanical recovery or enzyme leakage, suggesting that maintenance of tissue ascorbate level is not the cause, but the result of the protective effects of nitecapone against cardiac ischemia-reperfusion injury. The iron-chelating effect of nitecapone was also tested. It was confirmed, using electron spin resonance, that 50 microM nitecapone chelates the same concentration of iron released from the heart into the coronary effluent. Hence, the iron-chelating ability of nitecapone may be responsible, at least in part, for its cardioprotective effects in ischemia-reperfusion injury. Topics: Animals; Antioxidants; Ascorbic Acid; Catechol O-Methyltransferase Inhibitors; Catechols; Drug Interactions; Enzyme Inhibitors; Free Radical Scavengers; Iron Chelating Agents; Male; Myocardial Ischemia; Myocardial Reperfusion Injury; Pentanones; Rats; Rats, Sprague-Dawley | 1995 |
Hypoxic preconditioning preserves antioxidant reserve in the working rat heart.
The aim was to examine whether intracellular antioxidants play a role in myocardial preservation following hypoxic preconditioning.. Isolated working rat hearts were subjected to 30 min ischaemia and 30 min reperfusion. Control hearts were compared to hearts preconditioned with 10 min hypoxia. Left ventricular function and lactate dehydrogenase (LDH) release were measured in each group. Ascorbate dependent (ADAR) and thiol dependent (TDAR) components of the endogenous myocardial antioxidant reserve were assessed using electron spin resonance spectroscopy.. a Hypoxic preconditioning had no effect on left ventricular function after 10 min reoxygenation. During reperfusion, the hypoxically preconditioned hearts had a significantly increased survival rate, aortic flow, developed pressure, and dP/dtmax, and a reduced lactate dehydrogenase release, compared to non-preconditioned controls (P < 0.05). Preconditioned hearts also had significantly higher preservation of baseline ADAR (79%) and TDAR (96%) compared with control hearts, (70%) and (77%), respectively (P < 0.05).. Hypoxic preconditioning enhances functional recovery and reduces cell necrosis following global ischaemia in the working rat heart. This phenomenon may, in part, be mediated through enhanced ascorbate and thiol components of the antioxidant reserve. Topics: Animals; Antioxidants; Ascorbic Acid; Electron Spin Resonance Spectroscopy; Heart; L-Lactate Dehydrogenase; Male; Myocardial Infarction; Myocardial Ischemia; Myocardial Reperfusion; Myocardium; Perfusion; Rats; Rats, Sprague-Dawley; Sulfhydryl Compounds; Time Factors | 1995 |
The roles of reactive oxygen species and endogenous opioid peptides in ischemia-induced arrhythmia of isolated rat hearts.
Although the formation of oxygen-derived free radicals (or reactive oxygen species; ROS) and the release of endogenous opioid peptides (EOP) have been independently reported to be the major arrhythmogenic factors in ischemic hearts, possible relations between these two factors have seldom been investigated. Thus, we studied whether the ROS and EOP were related in the progression of ischemia-induced arrhythmias. Isolated rat hearts perfused in the Langendorff mode were treated with dynorphin A1-13 (kappa EOP receptor agonist), and/or allopurinol (xanthine oxidase inhibitor), before the onset of ischemia induced by ligating the left coronary arteries. Ischemic period lasted for 30 min, during which cardiac rhythms were recorded. At the end of ischemia, hearts were analyzed for the glutathione and ascorbate levels. Allopurinol (100 nmoles/heart) was effective in reducing the severity of arrhythmia (arrhythmia score: Mean +/- SEM 3.00 +/- 0.80 for allopurinol, 5.75 +/- 0.41 for placebo, p < 0.01), while dynorphin (10 micrograms/heart) potentiated the arrhythmia (6.71 +/- 0.52, p < 0.05 vs. placebo). Coadministration of allopurinol and dynorphin was capable of reducing arrhythmia (5.57 +/- 0.65) when compared with the administration of dynorphin alone (6.71 +/- 0.52, p < 0.05). Tissue oxidative stress was evaluated by the concentrations of glutathione (GSH) and ascorbate. Allopurinol did not significantly elevate tissue GSH concentrations (1.46 +/- 0.05 mumoles/g wet wt) in ischemic hearts, while dynorphin alone significantly decreased the GSH concentrations (0.96 +/- 0.08, p < 0.05) when compared with the placebo (1.32 +/- 0.03). The dynorphin-induced GSH decrease cannot be reversed by coadministration with allopurinol (0.90 +/- 0.104). Allopurinol significantly elevated tissue ascorbate levels (0.16 +/- 0.01) when compared with placebo (0.10 +/- 0.01, p < 0.05). Interestingly, dynorphin alone also elevated the tissue ascorbate concentrations (0.16 +/- 0.02). Coadministration of allopurinol and dynorphin further spiked the ascorbate levels (0.28 +/- 0.05, p < 0.01). In conclusion, the results suggested that ischemia-induced arrhythmia mechanisms might involve the formation of superoxide and other ROS, which were probably generated from the release of EOP (or EOP/EOP receptor interactions). Superoxide, the formation of which can be inhibited by allopurinol that exerted antiarrhythmic effect, was probably scavenged by ascorbate in myocardial ischemia. The ROS r Topics: Allopurinol; Animals; Arrhythmias, Cardiac; Ascorbic Acid; Dynorphins; Female; Free Radicals; Glutathione; In Vitro Techniques; Models, Cardiovascular; Myocardial Ischemia; Opioid Peptides; Oxidative Stress; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species | 1995 |
Salicylate in the perfusate during ischemia/reperfusion prevented mitochondrial injury.
Salicylate is widely used as a stable trap for the highly reactive hydroxyl radical. The purpose of this study was to determine whether the addition of salicylate to hearts subjected to ischemia and reperfusion was able to prevent some injury. Salicylate was able to inhibit mitochondrial damage, and preserved ascorbate and alpha-tocopherol depletion due to ischemia/reperfusion in rat hearts. It did not prevent the elevation of low molecular weight iron. We conclude that salicylate functions as an antioxidant and afforded protection against ischemia and reperfusion. Topics: Animals; Antioxidants; Ascorbic Acid; Female; Mitochondria, Heart; Myocardial Ischemia; Myocardial Reperfusion Injury; Myocardium; Perfusion; Phosphorylation; Rats; Rats, Sprague-Dawley; Sodium Salicylate; Vitamin E | 1994 |
Antioxidant supplementation partially protects against myocardial mitochondrial ischemia/reperfusion injury, but ascorbate in the perfusate prevented the beneficial effect.
This study was undertaken to investigate whether prior antioxidant supplementation had a beneficial effect on subsequent myocardial ischemic/reperfusion injury and whether addition of ascorbate during ischemia/reperfusion had any effect. Supplementation with antioxidants resulted in elevated concentrations of myocardial alpha-tocopherol, but not of ascorbate. Combined supplementation with alpha-tocopherol, beta-carotene and ascorbic acid gave the highest myocardial alpha-tocopherol concentration. Hearts of rats supplemented with antioxidants was partially protected to ischemia/reperfusion as indicated by the mitochondrial function. However, addition of ascorbate during ischemia/reperfusion nullified this protective effect. Topics: Administration, Oral; Animals; Antioxidants; Ascorbic Acid; Female; Iron; Mitochondria, Heart; Myocardial Ischemia; Myocardial Reperfusion Injury; Myocardium; Oxidation-Reduction; Perfusion; Phosphorylation; Rats; Rats, Sprague-Dawley; Vitamin E | 1994 |
Effects of natural antioxidant ginkgo biloba extract (EGB 761) on myocardial ischemia-reperfusion injury.
Recently, it was reported that Ginkgo biloba extract (EGb 761), which is known to have antioxidant properties, also has antiarrhythmic effects on cardiac reperfusion-induced arrhythmias. In the present study, effects of EGb 761 on cardiac ischemia-reperfusion injury were investigated from the point of view of recovery of mechanical function as well as the endogenous antioxidant status of ascorbate. Isolated rat hearts were perfused using the Langendorff technique, and 40 min of global ischemia were followed by 20 min of reperfusion. EGb 761 improved cardiac mechanical recovery and suppressed the leakage of lactate dehydrogenase (LDH) during reperfusion. Furthermore, EGb 761 diminished the decrease of myocardial ascorbate content after 40 min of ischemia and 20 min of reperfusion. Interestingly, EGb 761 also suppressed the increase of dehydroascorbate. These results indicate that EGb 761 protects against cardiac ischemia-reperfusion injury and suggest that the protective effects of EGb 761 depend on its antioxidant properties. Topics: Analysis of Variance; Animals; Antioxidants; Ascorbic Acid; Dehydroascorbic Acid; Electron Spin Resonance Spectroscopy; Ginkgo biloba; Heart; In Vitro Techniques; L-Lactate Dehydrogenase; Male; Myocardial Ischemia; Myocardium; Plant Extracts; Rats; Rats, Sprague-Dawley; Reperfusion; Reperfusion Injury; Time Factors | 1994 |
Ascorbyl free radical as a real-time marker of free radical generation in briefly ischemic and reperfused hearts. An electron paramagnetic resonance study.
The role of free radicals in myocardial reperfusion injury remains controversial. We have developed a new method using ascorbyl free radical (AFR) as a real-time, quantitative marker of free radical generation during myocardial reperfusion. A total of 35 dogs were studied. Twelve open-chest dogs underwent either 5 minutes (n = 5) or 20 minutes (n = 7) of coronary artery occlusion and 30 minutes of reperfusion. Seven additional animals undergoing 20 minutes of coronary occlusion also received the antioxidant enzymes superoxide dismutase and catalase, beginning 10 minutes before occlusion through the end of reperfusion. Exogenous ascorbate was infused intravenously, and the concentration of AFR in the great cardiac vein was continuously measured by electron paramagnetic resonance spectroscopy. Preocclusion AFR concentration was similar in the three groups. Upon reperfusion, AFR rose significantly in each animal group (P < .05). However, the AFR rise in the 20-minute-occlusion group, 38 +/- 17%, was significantly greater than in the 5-minute-occlusion group, 27 +/- 14% (P < .002). In addition, in the animals that received superoxide dismutase and catalase, the rise in the AFR was markedly attenuated, 13 +/- 6% (P < .002). Two dogs that received ascorbate but did not undergo coronary artery occlusion/reperfusion sequences showed no change in coronary venous AFR signal, indicating the stability of the signal over time. Five dogs received ascorbate while undergoing interventions to alter coronary venous flow: intravenous saline, dobutamine, dipyridamole, and nitroglycerin. Coronary venous AFR changes were minimal despite large coronary flow alterations, indicating that the AFR signal is independent of changes in coronary venous flow.(ABSTRACT TRUNCATED AT 250 WORDS) Topics: Animals; Ascorbic Acid; Dogs; Electron Spin Resonance Spectroscopy; Free Radicals; Myocardial Ischemia; Myocardial Reperfusion | 1994 |
Diet and incident ischaemic heart disease: the Caerphilly Study.
The Caerphilly Prospective Ischaemic Heart Disease (IHD) Study is based on a sample of 2512 men aged 45-59 years when first seen. Nutrient intakes, estimated using a self-administered semi-quantitative food frequency questionnaire, are available for 2423 men (96%). Amongst these, 148 major IHD events occurred during the first 5 years of follow-up. Associations were examined between these events and baseline diet. Incident IHD (new events) was negatively associated with total energy intake: men who went on to experience an IHD event had consumed 560 kJ (134 kcal)/d (6%) less at baseline than men who experienced no event (P = 0.01). The relative odds of an IHD event was 1.5 among men in the lowest fifth of energy intake, compared with 1.3, 1.2, 0.9 and 1.0 respectively for the other four fifths (P < 0.05). The difference in energy intake was reflected in lower intakes of every nutrient examined. When expressed as a percentage of total energy, mean intakes of men who experienced an IHD event were virtually identical to those of men who did not. There was some evidence suggesting a positive association between total fat intake and IHD risk, but the trend was not consistent and not statistically significant. There was no association for animal fat. Alcohol consumption was negatively associated with subsequent IHD, but only in men who already had evidence of IHD at baseline (P < 0.05). Dietary fibre, particularly from fruit and vegetables, was 7% lower in men who had an incident IHD event (P < 0.05), but the difference was not independent of total energy. There was a trend of increasing IHD risk with decreasing vitamin C intake, the relative odds of an IHD event being 1.6 among men in the lowest one-fifth of the vitamin C distribution, but this was not statistically significant. Topics: Age Factors; Ascorbic Acid; Body Mass Index; Diet; Diet Surveys; Dietary Fats; Dietary Fiber; Energy Intake; Humans; Longitudinal Studies; Male; Middle Aged; Myocardial Ischemia; Prospective Studies; Smoking; Wales | 1993 |
Poor plasma status of carotene and vitamin C is associated with higher mortality from ischemic heart disease and stroke: Basel Prospective Study.
Previous cross-cultural comparisons of the mortality from ischemic heart disease in European communities with associated plasma levels of essential antioxidants have revealed strong inverse correlations for vitamin E and relatively weak correlations for other antioxidants. Similarly, in a case-control study in Edinburgh low plasma levels of vitamin E were significantly associated with an increased risk of previously undiagnosed angina pectoris whereas low levels of other essential antioxidants lacked statistical significance. The current Basel Prospective Study is particularly well suited to elucidate the impact of antioxidants other than vitamin E. In this population (which was recently evaluated regarding cancer mortality) the plasma levels of vitamins E and A are exceptionally high and above the presumed threshold level of risk for ischemic heart disease. The present 12-year follow-up of cardiovascular mortality in this study reveals a significantly increased relative risk of ischemic heart disease and stroke at initially low plasma levels of carotene (< 0.23 mumol/l) and/or vitamin C (< 22.7 mumol/l), independently of vitamin E and of the classical cardiovascular risk factors. Low levels of both carotene and vitamin C increase the risk further, in the case of stroke even with significance for overmultiplicative interaction. In conclusion, in cardiovascular disease independent inverse correlations may exist for every major essential antioxidant although the latter can also interact synergistically. Therefore future intervention trials of antioxidants in the prevention of ischemic heart disease should primarily test the simultaneous optimization of the status of all principal essential antioxidants. Topics: Adult; Antioxidants; Ascorbic Acid; Ascorbic Acid Deficiency; Carotenoids; Cerebrovascular Disorders; Cohort Studies; Comorbidity; Humans; Male; Myocardial Ischemia; Proportional Hazards Models; Prospective Studies; Risk; Risk Factors; Switzerland; Vitamin A; Vitamin E | 1993 |
Inverse correlation between essential antioxidants in plasma and subsequent risk to develop cancer, ischemic heart disease and stroke respectively: 12-year follow-up of the Prospective Basel Study.
There is accumulating evidence that free radicals may contribute to various diseases such as cancer or cardiovascular disease. Possible health hazards can to some extent be prevented by the body's multilevel defense system against free radicals, which comprises, besides others, antioxidant vitamins. The 12-year mortality follow-up of 2,974 participants of the Basal Study allowed to test the hypothesis that low antioxidant vitamin plasma concentrations (vitamin A, C, E and carotene) were associated with increased death from cancer of various sites and death from atherosclerosis such as ischemic heart disease and stroke, respectively. For the analysis 204 cancer cases, 132 fatalities from ischemic heart disease (IHD) and 31 deaths from cerebral vascular disease were available. Cancer mortality. Overall mortality from cancer was associated with low mean plasma levels of carotene adjusted for cholesterol (p less than 0.01) and of vitamin C (p less than 0.01). Bronchus and stomach cancers were associated with a low mean plasma carotene level (p less than 0.01). Subjects with subsequent stomach cancer had also lower mean vitamin C and lipid-adjusted vitamin A levels than survivors (p less than 0.05). Calculating the relative risk with exclusion of mortality during the first two years of follow-up, low plasma carotene was associated with an increased risk for bronchus cancer (RR 1.8, p less than 0.05), and the small number of stomach cancer cases (RR 2.95, p less than 0.05) low plasma levels of carotene and vitamin A with all cancer types (RR 2.47, p less than 0.01), and low plasma retinol in older subjects (greater than 60 years) with lung cancer (RR 2.17, p less than 0.05). Studies in other cohorts with a poor vitamin E status revealed an increased risk of subsequent cancer at low vitamin E levels as well. It is concluded that low plasma levels of all major essential antioxidants are associated with an increased risk of subsequent cancer mortality. Cardio-vascular mortality. Plasma carotene concentration below quartile 1 was associated with an increased risk for IHD (RR 1.53, p = 0.02). The same was true for low levels of both carotene and vitamin C (RR = 1.96, p = 0.022). The risk of cerebrovascular death was elevated in subjects with low carotene in the presence of low vitamin C plasma concentration (RR 4.17, p less than 0.01). These data confirm and extend recent findings on an inverse correlation of beta-carotene and vitamin C respectively to CVD.(ABSTRACT Topics: Antioxidants; Ascorbic Acid; Cardiovascular Diseases; Carotenoids; Cerebrovascular Disorders; Cholesterol; Female; Follow-Up Studies; Free Radicals; Humans; Male; Myocardial Ischemia; Neoplasms; Prospective Studies; Risk Factors; Switzerland; Vitamin A; Vitamin E; Vitamins | 1992 |
[Study on the physiopathology of myocardial ischemia and cardiac revascularization. II. Behavior of blood glutathione and ascorbic acid after cardiac revascularization].
Topics: Ascorbic Acid; Coronary Artery Disease; Glutathione; Humans; Myocardial Infarction; Myocardial Ischemia; Myocardial Revascularization | 1959 |
[Study on the physiopathology of myocardial ischemia and of cardiac revascularization. I. Behavior of blood glutathione and ascorbic acid after experimental myocardial infarct].
Topics: Ascorbic Acid; Coronary Artery Disease; Glutathione; Humans; Myocardial Infarction; Myocardial Ischemia; Myocardial Revascularization | 1959 |