ascorbic-acid and Pulmonary-Edema

Paraquat poisoning in Germany is rare. Because plasma levels do not necessarily match the ingested amount of paraquat, repeated measurement of plasma levels is imperative. There is a large potential in the prehospital phase to improve prognosis: further resorption must be terminated by rigorous charcoal administration and early tracheal intubation if necessary. Because paraquat can be resorbed by dermal contact, steps to ensure sufficient protection of emergency medical personnel must be taken.As soon as further resorption has been prevented sufficiently, forced diuresis, renal replacement therapy, and hemoperfusion can be of help, but still remain controversial. To reduce pulmonary fibrosis, inspiratory oxygen concentrations must be adjusted to the minimal amount needed to ensure satisfactory tissue oxygenation. Data supporting the advantageous use of cyclophosphamide combined with methylprednisolone for the treatment of pulmonary fibrosis were recently published. Since the toxic mechanism implies a mismatch of oxidants and anti-oxidants, co-administration of ascorbic acid and N-acetylcysteine are simple treatments with few side effects.

Topics: Acetylcysteine; Acute Kidney Injury; Acute Lung Injury; Adult; Antioxidants; Ascorbic Acid; Combined Modality Therapy; Conscious Sedation; Cooperative Behavior; Critical Care; Dose-Response Relationship, Drug; Emergency Medical Services; Esophagoscopy; Esophagus; Gastric Mucosa; Hemofiltration; Herbicides; Humans; Interdisciplinary Communication; Intermittent Positive-Pressure Ventilation; Intestinal Mucosa; Male; Metabolic Clearance Rate; Oxygen Inhalation Therapy; Paraquat; Prognosis; Pulmonary Edema; Suicide, Attempted

To determine whether vitamin C in the first three days postpartum reduces pulmonary oedema (PE) assessed by lung ultrasound in patients with severe preeclampsia.. Randomised, placebo-controlled, double-blind trial.. Tertiary perinatal centre.. Consecutively admitted patients with singleton pregnancies complicated by severe preeclampsia.. Thirty-four patients received vitamin C (1.5 g/6 h) (n = 17) or placebo (n = 17) at days 1, 2, and 3 postdelivery. Mann-Whitney-U test was used to compare vitamin C vs placebo groups. A p ≤ 0.05 was considered statistically significant.. Lung ultrasound was performed once daily in the first three days following delivery. Echo Comet Score (ECS) on day 1 postdelivery was the primary outcome studied and was obtained using the 28-rib interspaces technique. ECS on days 2 and 3 postdelivery were secondary outcomes.. There was no significant difference in ECS on day 1 (median 23 (inter-quartile range (IQR) 21-61) vs 18 (IQR 8-35); p = 0.31). All ultrasound examinations on day 1 were performed within six hours from delivery. On days 2 and 3, ECS was significantly lower in vitamin C group compared to placebo (8 (IQR 3-14) vs 35 (IQR 15-78); p = 0.03 and 5 (IQR 3-10) vs 18 (IQR 18-44); p = 0.04, respectively).. A single dose of intravenous vitamin C did not reduce PE in postpartum patients with severe preeclampsia on day 1 after delivery. Repeated doses, however, seem to have a delayed effect with a reduction in PE detected on ultrasound on days 2 and 3 following delivery.. This trial is registered at ClinicalTrials.gov: ID NCT03451266 (https://clinicaltrials.gov/ct2/show/NCT03451266?term=NCT03451266&draw=2&rank=1).

Topics: Ascorbic Acid; Double-Blind Method; Female; Humans; Lung; Pre-Eclampsia; Pregnancy; Pulmonary Edema

Topics: Ascorbic Acid; Double-Blind Method; Female; Humans; Postpartum Period; Pre-Eclampsia; Pregnancy; Pulmonary Edema

Topics: Ascorbic Acid; Double-Blind Method; Female; Humans; Peripartum Period; Pre-Eclampsia; Pregnancy; Pulmonary Edema

not available.

Topics: Ascorbic Acid; Clinical Trials as Topic; COVID-19; Humans; Influenza, Human; Pulmonary Edema; Vitamin D; Vitamin D Deficiency; Vitamins

The objectives of this study were to compare the protective effects of ascorbic acid and iloprost on lung injury caused by ischemia reperfusion (I/R) of the lower extremities of rats. Wistar albino rats (n = 34) were divided into five groups. In the I/R group (n = 6), the aorta was cross-clamped for 3 hr, followed by 1 hr of reperfusion. In the vitamin C group (n = 8), animals were pretreated with 100 mg/kg ascorbic acid via the left jugular vein before aortic cross-clamping. In the iloprost group (n = 8), animals were pretreated with 20 ng/(kg x min) iloprost by constant intravenous infusion via the left jugular venous cannula. In the sham group (n = 6), the abdomen was left open at the same period and a juguler venous line was established. In the control group (n = 6), lungs were removed and blood samples taken immediately after sternotomy. No treatment was given in this group. After both lungs were removed, biochemical parameters were measured and histopathological evaluation was made. Although the arterial blood pO2 and HCO3 levels were statistically significantly high in both the vitamin C and iloprost groups compared to the I/R group, plasma malondialdehyde (MDA) levels were significantly low. Meanwhile, the MDA levels in the lung tissue were significantly low in the vitamin C group compared to the I/R group. The MDA level in the lung tissue in the iloprost group was also low compared to the I/R group, but it was not statistically significant. The lungs of the I/R group displayed intense interstitial leukocytic infiltration in histopathological examination compared to the other groups. Pretreatment of animals with iloprost and vitamin C significantly decreased the pulmonary injury characterized by decreased plasma leukocyte sequestration. The results suggest that both vitamin C and iloprost are useful agents for attenuating the lung injury caused by increased oxidative stress and neutrophil accumulation after a period of I/R of the lower extremities.

Topics: Animals; Aorta, Abdominal; Ascorbic Acid; Constriction; Disease Models, Animal; Free Radical Scavengers; Iloprost; Lipid Peroxidation; Lung; Neutrophils; Platelet Aggregation Inhibitors; Pulmonary Edema; Rats; Rats, Wistar; Reperfusion Injury

Amyloidosis results from protein infiltration of the extracellular space of organs and tissues. Several amyloidosis proteins have been identified. Protein AL, (deriving from immunoglobulin light chain), protein AA and prealbumin are the most involved in this disease. When AL amyloidosis involves the heart, the illness is often terminal. Most clinical symptoms are heart failure and arrhythmia or block conduction. This case was characterised by the unusual combination of hypertension and amyloidosis. The diagnosis suggested by the echocardiographic but was confirmed by the damaged organ's biopsy. The present case concerns a young woman, who has hypertension and a pulmonary oedema. The echocardiographic scan showed a septal hypertrophy with a shining and granite-like aspect which is compatible with heart amyloidosis. Systolic and diastolic disorder with mitral and aortic regurgitation were also revealed. The kidney and rectum biopsies confirmed amyloidosis AL of the Kappa dysglobulinemia type, without extraosseous plasmocytoma. The heart and kidney failure symptoms disappeared after treatment with diuretics and ACE inhibitors.

Topics: Adult; Amyloidosis; Angiotensin-Converting Enzyme Inhibitors; Ascorbic Acid; Biopsy; Cardiomegaly; Colchicine; Diuretics; Echocardiography; Female; Heart Failure; Heart Valve Diseases; Humans; Hypertension; Immunoglobulin kappa-Chains; Nephritis; Paraproteinemias; Pulmonary Edema; Radiography; Rectum

Inflammation-induced disease as seen with trauma and infection can lead to increased lung oxidant activity resulting in cell membrane lipid peroxidation. Acute zymosan-induced peritonitis in rats produces lung inflammation, edema, and lipid peroxidation. We determined whether administered alpha-tocopherol (vitamin E), the key antioxidant protection against cell membrane lipid peroxidation, would improve this process.. Male Wistar rats were given 0.75 mg/kg of intraperitoneal zymosan, volume resuscitated, monitored, and killed at 4 or 24 hours. Lung histologic changes and levels of conjugated dienes, a marker of lipid peroxidation, were used to monitor injury. The levels of vitamin E, vitamin C, and catalase were used to monitor antioxidant defenses. The effect of administering alpha-tocopherol (50 mg/kg) by gavage immediately after zymosan on the degree of the lung injury was then determined.. Twenty-four hours after zymosan was administered, the vitamin E levels in plasma were significantly decreased, but lung tissue vitamin E levels were maintained, whereas tissue catalase and vitamin E levels decreased. Lung tissue-conjugated diene levels, alveolar edema, and neutrophil count were significantly increased. alpha-Tocopherol treatment increased the postzymosan plasma vitamin E levels by 50%. Lung tissue vitamin E levels did not increase; however, the degree of lung injury and lipid peroxidation was significantly attenuated. Tissue catalase levels were also maintained.. We conclude that alpha-tocopherol given at the onset of a progressing inflammatory injury can protect the lung from oxidant damage and attenuate the degree of lung injury.

Topics: Acute Disease; Animals; Ascorbic Acid; Catalase; Lipid Peroxidation; Lung; Male; Peritonitis; Pulmonary Edema; Rats; Rats, Wistar; Vitamin E; Zymosan

Acute zymosan-induced peritonitis in rats produces lung inflammation and lipid peroxidation. The effect of this process on plasma and lung tissue ascorbic acid was determined, as was the effect of infusing 150 mg/kg of ascorbic acid immediately after zymosan on the degree of lung insult. Ascorbic acid levels were significantly decreased in plasma and lung tissue at 24 h after zymosan, and lung tissue conjugated diene and neutrophil content was also significantly increased. Vitamin C infusion increased postzymosan plasma levels by 50% over normal control levels. However, lung tissue ascorbic acid was still decreased, and no decrease in the lung injury process was noted. Added ascorbic acid also did not prevent a decrease in plasma vitamin E with the peritonitis. We conclude that the amount of ascorbic acid given in this study did not diminish the lung oxidant inflammatory changes. An insufficient dose or inadequate time for plasma ascorbic acid to equilibrate with the lung cytosol are possible explanations for the lack of attenuation of lung oxidant stress.

Topics: Acute Disease; Animals; Antioxidants; Ascorbic Acid; Ascorbic Acid Deficiency; Inflammation; Lipid Peroxidation; Lung; Male; Oxidation-Reduction; Peritonitis; Pulmonary Edema; Rats; Rats, Wistar; Vitamin E; Vitamin E Deficiency; Zymosan

Oxidative stress has been implicated in the adult respiratory distress syndrome (ARDS). In this study, we determined the levels of selected antioxidants in the plasma of 25 patients with ongoing ARDS and 16 healthy control subjects. We also examined these plasmas and pulmonary edema fluid of ARDS patients for lipid hydroperoxides. Both ascorbate and ubiquinol-10 concentrations in ARDS plasma were significantly lower than in normal plasma. alpha-Tocopherol concentrations, when standardized to total plasma cholesterol, were not lower in ARDS patients than in normal subjects. A pattern of antioxidant levels virtually identical to that observed in ARDS plasma was obtained after in vitro incubation of healthy plasma with stimulated polymorphonuclear leukocytes: very low ascorbate, decreased ubiquinol-10, and unchanged alpha-tocopherol concentrations. Nanomolar concentrations of lipid hydroperoxides were found in pulmonary edema fluid of ARDS patients, but not in plasma, nor in the plasma of healthy individuals, when a sensitive and selective chemiluminescence assay for hydroperoxides was used. ARDS patients also showed significant decreases in plasma levels of cholesterol esters in conjunction with discoidal high-density lipoprotein profiles, indicating a decrease in lecithin-cholesterol acyltransferase activity. We conclude that ARDS is associated with oxidative stress, possibly exerted by oxidants released from activated phagocytic leukocytes, and major changes in plasma cholesterol metabolism.

Topics: Adult; Aged; Antioxidants; Ascorbic Acid; Cholesterol; Cholesterol Esters; Exudates and Transudates; Female; Humans; Lipid Peroxides; Luminescent Measurements; Male; Middle Aged; Neutrophils; Oxidation-Reduction; Oxygen; Pulmonary Edema; Respiratory Distress Syndrome; Tetradecanoylphorbol Acetate; Ubiquinone; Vitamin E

Loss of ascorbic acid from lung and pulmonary edema were produced in mice by intravenous injection of either adrenaline or noradrenaline (5 mumol/kg). While adrenalectomy performed before noradrenaline administration reduced the degree of pulmonary edema, a prior dose of hexamethonium accentuated this effect. Given alone, hexamethonium caused both loss of ascorbic acid and pulmonary edema. The results show that although endogenous catecholamines can potentiate the pulmonary edema produced by either adrenaline or noradrenaline, they play no specific role in the ascorbic acid loss. The evidence suggests that lung ascorbic acid levels are decreased following the development of pulmonary edema, irrespective of how it was caused.

Topics: Adrenal Glands; Animals; Ascorbic Acid; Catecholamines; Ganglionic Blockers; Hexamethonium Compounds; Lung; Male; Mice; Organ Size; Pulmonary Edema; Stimulation, Chemical; Water

Topics: Adrenergic alpha-Antagonists; Adrenergic beta-Antagonists; Animals; Ascorbic Acid; Body Weight; Bucladesine; Catecholamines; Epinephrine; Histamine; Isoproterenol; Lung; Male; Mice; Norepinephrine; Organ Size; Phenoxybenzamine; Phenylephrine; Propranolol; Pulmonary Edema; Serotonin

Topics: Adrenal Insufficiency; Ascorbic Acid; Autonomic Nervous System Diseases; Blood Circulation; Communicable Diseases; Cortisone; Desoxycorticosterone; Encephalitis; Flavonoids; Humans; Liver; Pathology; Pulmonary Edema; Rutin; Water-Electrolyte Balance

Topics: Animals; Ascorbic Acid; Hydrocortisone; Mice; Ozone; Pulmonary Edema; Vitamins

Topics: Animals; Ascorbic Acid; Humans; Pulmonary Edema; Rabbits; Tuberculosis; Vitamins