phosphocreatine and Acute-Disease

Topics: Acute Disease; Coronary Artery Disease; Cytokines; Humans; Inflammation; Myocardial Ischemia; Phosphocreatine

The purpose of the study was to characterize the functional and metabolic adjustments of a myocardial region subjected to low-flow ischemia. In addition, studies tested whether such myocardium retains an inotropic reserve.. Anesthetized swine were studied in which the left anterior descending coronary artery was cannulated and perfused at a constant low level causing regional contractile dysfunction (sonomicrometry for wall thickness) and the appearance of metabolic indicators of ischemia (decrease in creatine phosphate and lactate production) with only slight loss of ATP and glycogen (transmural biopsies). After 85 minutes of low-flow ischemia, dobutamine was infused into the hypoperfused artery as an inotropic challenge. Coronary hypoperfusion for 5 minutes resulted in a 54% reduction of regional systolic wall thickening, reversal of lactate consumption to lactate production, and a significant decrease in creatine phosphate. Subendocardial blood flow was reduced from 0.62 +/- 0.11 (+/- SD) to 0.16 +/- 0.07 mL.min-1.g-1. Prolonged hypoperfusion for 85 minutes resulted in no further change in regional blood flow but a partial recovery of metabolic parameters. Dobutamine infusion after 85 minutes of hypoperfusion increased regional myocardial work. However, again lactate production was significantly increase and creatine phosphate was decreased. Regional coronary hypoperfusion produces a downregulation of regional contractile function in proportion to the blood flow decrease. With prolonged hypoperfusion, after the initial adjustment phase, there is little further change in function, and metabolic markers of ischemia improve. Although the ischemic downregulated myocardium retains a significant inotropic reserve, primarily anaerobic energy production is utilized.. These data are consistent with downregulation being a protective mechanism for the ischemic myocardium to restore an energy supply-demand balance in the face of reduced blood flow. Inotropic stimulation of the downregulated myocardium enhances regional function but at the cost of worsening its metabolic status. Thus, inotropic stimulation of the hypoperfused and downregulated myocardium is probably detrimental to long-term viability.

Topics: Acute Disease; Adenosine Triphosphate; Animals; Coronary Circulation; Dobutamine; Glycogen; Heart; Myocardial Contraction; Myocardial Ischemia; Myocardium; Phosphocreatine; Swine; Time Factors

On the basis of the data from the literature and own studies the genesis of acute cardiac insufficiency has been shown to be directly associated with a sharp decline in the effectiveness of intracellular energy transportation. A challenging factor in the transformation of the pathological process into acute cardiac insufficiency may consist in one of the three main types of influence: (1) hypoxia of the myocardium, (2) effects causing disorders in the calcium metabolism, and (3) additional mechanical loads on the already affected myocardium. The pattern of the observed ultrastructural changes may be used to a certain extent for the judgement on the type of effect which was most important in the genesis of acute cardiac insufficiency.

Topics: Acute Disease; Adenosine Triphosphate; Animals; Calcium; Energy Metabolism; Humans; Microscopy, Electron; Mitochondria, Heart; Myocardial Contraction; Myocardial Infarction; Myocardium; Phosphocreatine; Rabbits

Sickle cell disease (SCD) is characterized by painful vaso-occlusive crisis. While there are several metabolic abnormalities potentially associated with muscular ischemia-reperfusion cycles that could be harmful in the context of SCD, the metabolic consequences of such events are still unknown. Ten controls (HbAA), thirteen heterozygous (HbAS), and ten homozygous (HbSS) SCD mice were submitted to a standardized protocol of rest-ischemia-reperfusion of the left leg during which adenosine triphosphate, phosphocreatine, and inorganic phosphate concentrations as well as intramuscular pH were measured using phosphorous magnetic resonance spectroscopy (MRS). Forty-eight hours later, skeletal muscles were harvested. Oxidative stress markers were then measured on the tibialis anterior. At the end of the ischemic period, HbSS mice had a lower pH value as compared with the HbAA and HbAS groups (

Topics: Acute Disease; Adenosine Triphosphate; Anemia, Sickle Cell; Animals; Antioxidants; Hydrogen-Ion Concentration; Ischemia; Magnetic Resonance Spectroscopy; Mice; Muscle, Skeletal; Oxidative Stress; Phosphocreatine; Reperfusion Injury; Rest; Time Factors

Phosphocreatine (PCr) mobilizes high-energy phosphates in cardiac muscles, which is potentially useful as a cardioprotective agent in patients with spinal cord injury (SCI). The cardioprotective effects of PCr on myocardial cell ultrastructure and calcium-sensing receptor (CaSR) expression following high-level spinal cord injury (SCI) were investigated. Healthy adult male Sprague-Dawley (SD) rats (n=54) weighing 250-300 g were subjected to C7 SCI injury by Allen's method with or without treatment by abdominal injection of PCr (200 mg/kg) at 6, 12, 24 or 48 h (SCI + treatment and SCI-only groups, respectively; 6 rats/group/time point). Right apical tissues were sampled 2 h following each time interval. Surgeries without SCI were performed in 6 control rats (sham operation group). Cardiac troponin I (cTnI), serum creatine kinase (CK) and creatine kinase (CK-MB) levels were assessed automatically. Myocardial morphology was examined by transmission electron microscopy (TEM). Quantitative real‑time polymerase chain reaction (qRT-PCR) and western blot analysis were used to determine myocardial tissue calcium-sensing receptor (CaSR) mRNA and protein expression, respectively. Normal myocardial ultrastructure was observed in the sham operation group, while SCI-only groups exhibited progressive and extensive damage to myofibrils, sarcomere structure, mitochondrial membranes and vacuole structures, occasionally accompanied by punctured cell membranes, nuclear chromatin condensation and cavitation. SCI + treatment groups, however, exhibited significantly relieved ultrastructural abnormalities and reduced the levels of CaSR, cTnI, CK and CK-MB mRNA and protein expression at all time intervals (P<0.05). In the SCI rat model, PCr exhibited cardioprotection by relieving myocardial ultrastructural abnormalities and preserving the normal metabolic energy balance, including calcium regulation.

Topics: Acute Disease; Animals; Cardiotonic Agents; Creatine Kinase; Creatine Kinase, MB Form; Male; Myocytes, Cardiac; Necrosis; Phosphocreatine; Rats; Rats, Sprague-Dawley; Receptors, Calcium-Sensing; RNA, Messenger; Spinal Cord Injuries; Time Factors; Troponin I

Several neurochemical abnormalities have been reported in bipolar disorder (BD), but the exact mechanisms that underlie its pathophysiology remain to be elucidated. Proton magnetic resonance spectroscopy (1HMRS) allows in vivo measurements of certain neurometabolites in the human brain. 1HMRS was used to investigate the dorsolateral prefrontal cortex (DLPFC) in bipolar subjects during a manic or mixed phase. N-acetyl-L-aspartate (NAA), choline-containing molecules (Cho), creatine plus phosphocreatine (Cr) and myoinositol (Ino) were measured.. Ten bipolar patients (nine manic, one mixed), diagnosed by a semi-structured clinical interview (SCID), and ten age- and gender-matched healthy volunteers were studied. Absolute neurometabolites levels were measured from two 8 cm3 voxels placed in left and right DLPFC using a short TE 1HMRS method at 1.5 T. T1- and T2-weighted anatomical magnetic resonance imaging was performed to exclude any neuroanatomical abnormality.. No significant differences were found for NAA, Cho, Cr, Ino, NAA/Cr, Cho/Cr or Ino/Cr between patients and controls. Manic/mixed patients had significantly higher left-to-right myoinositol ratios in DLPFC (p = 0.044).. Increased left-to-right myoinositol ratios in the DLPFC in bipolar patients during acute mania may represent a dysfunction in the phosphoinositide-signaling pathway. Longitudinal studies with larger samples of unmedicated patients assessing pre- and post-treatment times will be required for further clarification of the time course of these abnormalities and the relationship with treatment effects.

Topics: Acute Disease; Adult; Antimanic Agents; Antipsychotic Agents; Aspartic Acid; Bipolar Disorder; Choline; Diagnostic and Statistical Manual of Mental Disorders; Female; Humans; Inositol; Magnetic Resonance Imaging; Male; Middle Aged; Patient Selection; Phosphocreatine; Prefrontal Cortex

Biopsies are difficult to perform in rodent heart transplant models without compromising the graft function and therefore other means to evaluate the grafts repeatedly and noninvasively are warranted. The goal of the present study was to measure changes in ratios of high energy phosphorus containing metabolites detected with in vivo 31Phosphorous Magnetic Resonance Spectroscopy ((31)P MRS) in a xenotransplantation model and to investigate if these ratios correlated to histological signs of acute xenograft rejection. Thirty-five heart transplantations were performed (NMRI-mice to Lewis (RT1(1)) rats). Thirteen heart transplants underwent repeated daily in vivo (31)P MRS measurements and 22 grafts were measured on any of 4 postoperative days and thereafter sacrificed for histology. A modified scoring system based on Billingham's criteria was used to stage the rejection process. The median graft survival was 3.0 +/- 0.44 (median +/- SD) days (n = 17). Significant differences, both overall and interday, could be calculated for the phosphocreatine (PCr)/beta-adenosine triphosphate (beta-ATP) ratios and for the rejection score. The decreases in PCr/beta-ATP ratios correlated significantly to the progressive acute rejection process in the sacrificed grafts (P = 0.01). Further studies are indicated to establish the potential of (31)P MRS in immunosuppressed recipients of vascularized xenotransplants with prolonged graft survival.

Topics: Acute Disease; Adenosine Triphosphate; Animals; Energy Metabolism; Graft Rejection; Heart Transplantation; Magnetic Resonance Spectroscopy; Male; Mice; Mice, Inbred Strains; Myocardial Contraction; Myocardium; Phosphocreatine; Phosphorus Isotopes; Postoperative Period; Rats; Rats, Inbred Lew; Transplantation, Heterologous; Transplantation, Heterotopic

1. Failure of muscle force during sustained fatiguing contraction is associated with myoelectrical and metabolic alterations. However, the inter-relationships between these two types of events remain unclear. The purpose of this study was to examine the effects of decreased oxygen availability during sustained contraction on myoelectrical and metabolic changes, thereby addressing the issue of fatigue. 2. 31P-Magnetic resonance spectra and surface electromyograms were simultaneously recorded in six subjects (three women and three men) performing isometric contraction of forearm flexor muscles sustained at 60% maximum value of force under aerobic or acute hypoxaemic conditions (inhalation of a gas mixture containing 12% O2). 3. The 5 min hypoxaemic rest preceding contraction did not affect the phosphocreatine level and pH value. Under both conditions of oxygen availability, the magnitude of metabolic changes remained similar and the duration of contraction was unaffected (similar workload). However, hypoxaemia significantly reduced the rate of changes in integrated surface electromyogram activity measured in the high-frequency band. Correlative analysis of magnetic resonance spectroscopy and surface electromyogram data shows that for a given surface electromyogram change, metabolic variations were always larger under hypoxaemic conditions. 4. These results suggest that hypoxaemia does not alter metabolic changes, i.e. decrease in pH and phosphocreatine during static contraction. The downward shift of the relationships between myoelectrical and metabolic changes under hypoxaemia points to the existence of a better excitation-contraction coupling in acute hypoxaemia compared with normoxia and this is indicative of an adaptative mechanism.

Topics: Acute Disease; Adult; Electromyography; Female; Forearm; Humans; Hydrogen-Ion Concentration; Hypoxia; Isometric Contraction; Magnetic Resonance Spectroscopy; Male; Middle Aged; Muscle Fatigue; Muscle, Skeletal; Phosphocreatine

Studies of intact hearts suggest that cardiac myocytes may have the ability to reversibly suppress metabolic activity and energy demand in states of regional hypoperfusion. However, an ability to suppress respiration in response to hypoxia has never been demonstrated in isolated myocytes. To test this, isolated embryonic chick cardiac myocytes were exposed to progressive hypoxia while their rate of O2 uptake and concentrations of lactate, ATP, ADP, AMP, and phosphocreatine were measured. Compared with the value obtained at an oxygen tension (PO2) of 120 Torr, cellular O2 uptake decreased by 28 +/- 14% (SD) at PO2 = 50 Torr and by 64 +/- 25% at PO2 = 20 Torr (P < 0.05). This decrease was similar after 1 min or 2 h of hypoxia, was sustained for 16 h, and was completely reversible within 2 min after reoxygenation. The reduction in O2 uptake was associated with a decrease in the rate of ATP turnover, but no change in adenine nucleotide or phosphocreatine concentrations. In myocytes adherent to glass cover-slips, O2 uptake and contractile motion were decreased after 30-60 min at 50 and 20 Torr, compared with normoxic values. O2 uptake also was significantly decreased at 50 and 20 Torr in myocytes incubated with N,N,N',N'-tetramethyl-p-phenylenediamine, which suggests that the catalytic activity of cytochrome-c oxidase was partially inhibited during hypoxia. In summary, these results demonstrate that embryonic chick cardiac myocytes can suppress their rates of ATP demand, ATP utilization, and O2 uptake during moderate hypoxia through a mechanism that involves a reversible inhibition of cytochrome-c oxidase. This mechanism may represent a protective response to cellular hypoxia.

Topics: Acute Disease; Adenine Nucleotides; Adenosine Triphosphate; Anaerobiosis; Animals; Cell Adhesion; Chick Embryo; Energy Metabolism; Glycolysis; Hypoxia; Myocardial Contraction; Myocardium; Osmolar Concentration; Oxygen Consumption; Phosphocreatine; Tetramethylphenylenediamine

Severely birth-asphyxiated human infants develop delayed ("secondary") cerebral energy failure, which carries a poor prognosis, during the first few days of life. This study tested the hypothesis that mild hypothermia after severe transient cerebral hypoxia-ischemia decreases the severity of delayed energy failure in the newborn piglet. Six piglets underwent temporary occlusion of the common carotid arteries and hypoxemia. Resuscitation was started when cerebral [phosphocreatine (PCr)]/[inorganic phosphate (Pi)] as determined by phosphorus magnetic resonance spectroscopy had fallen almost to zero and [nucleotide triphosphate (NTP)]/[exchangeable phosphate pool (EPP)] had fallen below about 30% of baseline. Rectal and tympanic temperatures were then reduced to 35 degrees C for 12 h after which normothermia (38.5 degrees C) was resumed. Spectroscopy results over the next 64 h were compared with previously established data from 12 piglets similarly subjected to transient cerebral hypoxia-ischemia, but maintained normothermic, and six sham-operated controls. The mean severity of the primary insult (judged by the time integral of depletion of [NTP]/[EPP]) was similar in the hypothermic and normothermic groups. In the normothermic group, [PCr]/[Pi] and [NTP]/[EPP] recovered after the acute insult and then fell again. Minimum values for these variables observed between 24 and 48 h were significantly higher in the hypothermic group and not significantly different from the control values (p < 0.05, analysis of variance). A large reduction in secondary energy failure relative to the extent of the primary insult was shown and no further fall in either [PCr]/[Pi] or [NTP]/[EPP] took place up to 64 h in the hypothermic piglets.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acute Disease; Animals; Animals, Newborn; Cerebral Cortex; Energy Metabolism; Hypothermia, Induced; Hypoxia, Brain; Ischemic Attack, Transient; Phosphates; Phosphocreatine; Swine

To analyze the advantages of proton magnetic resonance (MR) spectroscopic imaging in the evaluation of acute and subacute cerebral infarcts.. Metabolite maps of choline-containing compounds, total creatine consisting of creatine and phosphocreatine, N-acetyl aspartate (NAA), and lactate were obtained in 23 patients with acute and subacute cerebral infarctions 1-35 days after onset of symptoms. Maps were obtained with a 1.5-T MR system with 32 x 32 phase-encoding steps.. Distinct abnormal metabolite distributions could be detected in all lesions larger than 1 cm in diameter. In the center of infarcts with a diameter larger than the section thickness of 2 cm, NAA values decreased to 20% +/- 8 compared with contralateral brain as early as 1 day after onset of symptoms (P < .0001). Choline was reduced to 67% +/- 30 (not significant) and creatine to 51% +/- 22 (P = .0025). Large amounts of lactate were detected in all acute infarcts. Choline, creatine, and lactate values declined during the first 5 weeks after stroke.. MR spectroscopic imaging allows visualization of metabolic changes in stroke with a reasonable spatial resolution.

Topics: Acute Disease; Adult; Aged; Aged, 80 and over; Aspartic Acid; Brain; Cerebral Infarction; Choline; Creatine; Female; Humans; Lactates; Lactic Acid; Magnetic Resonance Spectroscopy; Male; Middle Aged; Phosphocreatine

To address the problem of the pathogenesis of diabetic neuropathy, rats were made diabetic by alloxan administration, and sciatic nerves were sampled for electrolyte and water content and levels of selected carbohydrates and intermediates in energy metabolism at 3, 6, and 26 weeks. Significant increases were seen in the nerve content of glucose, sorbitol, and fructose. Decreases of myo-inositol were not statistically significant. Glucose-6-phosphate was increased at all times; fructose-1,6-bisphosphate was elevated at 6 and 26 weeks. Nerve ATP and phosphocreatine levels were both increased concomitantly, as was the energy charge. Nerve lactate levels increased only at 26 weeks when plasma lactate levels were also high. Plasma ketone bodies were elevated throughout the 26-week experimental interval. It is postulated that ketone bodies were being used as alternative metabolic fuels in diabetic nerve, thereby causing inhibition of pyruvate oxidation and increased aerobic production of lactate. Increased plasma ketone body levels could also inhibit hepatic lactate uptake. There was no other evidence for hypoxia/ischemia. Lactate:pyruvate ratios did not differ from control values at any time in these ketotic hypoinsulinemic animals. Five major hypotheses have been proposed to explain the pathogenesis of diabetic neuropathy: 1) hypoxia/ischemia, 2) hyperglycemic pseudohypoxia, 3) myo-inositol deficiency, 4) fructose and polyol accumulation and osmotic disequilibrium, and 5) nonenzymatic glycation of macromolecules by fructose and glucose. The data obtained in this study seem to fit best with hypotheses 4 and perhaps 5.

Topics: Acute Disease; Adenosine Triphosphate; Animals; Carbohydrate Metabolism; Chronic Disease; Diabetes Mellitus, Experimental; Diabetic Neuropathies; Electrolytes; Energy Metabolism; Fructose; Glucose; Male; Peripheral Nervous System Diseases; Phosphocreatine; Polymers; Rats; Rats, Sprague-Dawley; Sciatic Nerve; Sorbitol

Metabolic consequences of hypothyroidism in adult human brain, despite neuropsychological symptoms, have not been reported. We used 31P nuclear magnetic-resonance spectroscopy of the frontal lobe to examine the effect of acute hypothyroidism on cerebral metabolism. Paired analysis showed that the phosphocreatine/inorganic-phosphate (PCr/Pi) ratio increased from a median of 2.04 (interquartile range 0.15) to 2.22 (0.25) after treatment with levothyroxine (p = 0.01). These reversible alterations in adult cerebral phosphate metabolism during acute hypothyroidism parallel PCr/Pi ratio changes described in skeletal muscle. This is the first direct evidence of cerebral metabolic effects of hypothyroidism on adult brain.

Topics: Acute Disease; Adult; Brain; Carcinoma; Energy Metabolism; Humans; Hypothyroidism; Magnetic Resonance Spectroscopy; Middle Aged; Phosphates; Phosphocreatine; Thyroid Neoplasms; Thyroidectomy; Thyroxine

Mammals react to acute hypoxia with an initial augmentation and a secondary depression of the respiratory rhythm generated by brain stem neuronal networks. To investigate the cytosolic level of energy rich phosphorus metabolites during these responses, we developed 31P nuclear magnetic resonance spectroscopy of the brain stem. Moderate hypoxia (paO2 = 40 mmHg, 2 min) caused a reversible 62 +/- 15% respiratory rhythm depression and decreased cytosolic phosphocreatine levels by 43 +/- 11% (p < 0.01, n = 7) without affecting adenosine triphosphate levels. Cellular metabolic depletion therefore contributes to the brain stem response to hypoxia, and appears to reflect adaptive mechanisms to limited oxygen availability in the brain stem.

Topics: Acute Disease; Adenosine Triphosphate; Anesthetics; Animals; Brain Stem; Energy Metabolism; Hypoxia, Brain; Magnetic Resonance Spectroscopy; Male; Phosphocreatine; Phosphorus; Rats; Rats, Sprague-Dawley; Respiration

In order to investigate the changes in phosphoglucose metabolism in acute experimental pancreatitis, the authors utilized the measuring cell NMR spectroscopy. The experimental pancreatitis had been evoked by both the method of ligature of lateral pancreas ducts and that of the duodenal blind loop. These methods evoke a morphological response, namely edematous and necrotizing pancreatitis. Gradual reduction of macroergic phosphate binds and augmentation of anorganic phosphates represent the principal change in NMR spectrum. The clinical picture provides evidence of the exhaustion of highly energetic phosphate compounds which are necessary for the maintenance of integrity of the pancreas tissue in acute experimental pancreatitis. The discussion includes the possibilities and limitations of the NMR spectroscopy.

Topics: Acute Disease; Adenosine Triphosphate; Animals; Female; Magnetic Resonance Spectroscopy; Male; Pancreas; Pancreatitis; Phosphocreatine; Rats; Rats, Wistar

We used 31P magnetic resonance spectroscopy to compare the response of rat skeletal muscle to three kinds of proton load. During exercise (tetanic sciatic nerve stimulation), protons from lactic acid were buffered passively and consumed by net hydrolysis of phosphocreatine (PCr). During recovery from exercise, the pH-dependent efflux of protons produced by PCr resynthesis could be partially inhibited by amiloride or 4,4'-diisothiocyanostilbene-2,2'-disulphonate (DIDS), implicating both sodium/proton and bicarbonate/chloride exchange, but was not inhibited by simultaneous respiratory acidosis. In early recovery, up to 30% of proton efflux was mediated by lactate/proton cotransport. During acute respiratory acidosis at rest, the eventual change in muscle pH was consistent with passive buffering and was unaffected by amiloride or DIDS, implying no significant contribution of proton fluxes.

Topics: 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid; Acidosis, Respiratory; Acute Disease; Adenosine Diphosphate; Amiloride; Animals; Buffers; Carbon Dioxide; Carbonates; Electric Stimulation; Hydrogen-Ion Concentration; Lactates; Lactic Acid; Magnetic Resonance Spectroscopy; Muscles; Phosphocreatine; Phosphorus; Physical Exertion; Rats; Rats, Wistar; Rest; Sciatic Nerve

The influence of graded leg muscle ischaemia on the adaptation to training and on the acute response to exercise was studied in healthy subjects. Graded ischaemia during supine exercise was induced by application of 50 mmHg external pressure on the legs. This procedure reduced leg blood flow by 16%, venous oxygen saturation by 12 percentage units, and markedly increased lactate release (p < 0.05 for all). One-legged training was performed during four weeks, 4 sessions per week. Each session started with one leg training for 45 min with reduced blood flow (ischaemic training). The contralateral leg, serving as a control, was then trained with an identical power-output profile for 45 min but without flow restriction (non-ischaemic training). Ischaemic training enhanced the adaptation to training. Peak oxygen uptake and time to fatigue increased more (p < 0.05) with ischaemic than with non-ischaemic training. Citrate synthase activity, capillaries per fibre, and glycogen content were greater (p < 0.05) in the trained than in the detrained state. In the ischaemically trained leg, the type IIb fibre proportion was lower (p < 0.05) and the I fibre proportion tended to be higher (p = 0.06) in the trained than in the detrained state. Maximum voluntary dynamic strength was decreased by 8% (p < 0.01) in the ischaemically trained leg, but was unaffected in the non-ischaemically trained leg. During acute ischaemic exercise, as compared to non-ischaemic exercise, there was a higher degree of glycogen depletion, a greater depletion of type II, but not of type I fibres, a greater electromyographic activity, higher catecholamine concentrations, lower intramuscular ATP and creatine phosphate content, and an increased nitric oxide formation as estimated by increased plasma nitrate content. In conclusion, the mechanisms underlying the potentiation of the adaptation to training by ischaemia are assumed to depend on the operation of stimuli which were amplified during acute ischaemic exercise.

Topics: Acute Disease; Adaptation, Physiological; Adenosine Triphosphate; Adolescent; Adult; Biopsy; Blood Flow Velocity; Blood Gas Analysis; Capillaries; Catecholamines; Citrate (si)-Synthase; Electromyography; Exercise Therapy; Glycogen; Humans; Ischemia; Lactates; Lactic Acid; Leg; Male; Models, Cardiovascular; Muscles; Nitric Oxide; Oxygen; Oxygen Consumption; Phosphocreatine

The hemodynamic effects of acute and long-term administration of creatine phosphate were studied in 23 patients with heart failure (NYHA classes II and III) under stabilized treatment. Acute creatine phosphate (5 g i.v.) induced a significant increase of the ejection fraction (FE) and of other parameters of cardiac contractility. Once these improvements of cardiac contractility were obtained by acute treatment, further significant increases in cardiac function were observed if treatment was continued for six days, i.e. telesystolic diameter and volume, as well as parietal stress were significantly reduced, and ejection fraction and shortening fraction were significantly increased. Creatine phosphate treatment has a favourable influence on the hemodynamics of patients with an obvious contractility deficit and chronic ischemia of the myocardium.

Topics: Acute Disease; Aged; Cardiomyopathy, Dilated; Chronic Disease; Drug Evaluation; Echocardiography; Female; Heart Failure; Hemodynamics; Humans; Male; Middle Aged; Myocardial Ischemia; Phosphocreatine

Magnetic resonance imaging and spectroscopy were performed in several types of muscular disorders. In acute stages, 31P spectra showed remarkable changes compared with normals, and T2-weighted MR images were most sensitive in delineating the pathology. Fatty degeneration of muscle in chronic diseases yielded high contrast in T1-weighted MRI and could be quantified by 1H-MRS including the chemically selective determination of proton T1 values. In order to evaluate true abundance rations of phosphorus metabolites, 31P relaxation times T1 of muscle were measured by localized inversion recovery.

Topics: Acute Disease; Adenosine Triphosphate; Adipose Tissue; Adult; Body Water; Chronic Disease; Energy Metabolism; Female; Humans; Image Processing, Computer-Assisted; Magnetic Resonance Imaging; Magnetic Resonance Spectroscopy; Male; Middle Aged; Muscles; Phosphates; Phosphocreatine; Polymyositis

The early time course after acute stroke of cerebral N-acetylaspartate, creatine and phosphocreatine, and compounds containing choline was studied in vivo by means of localized water-suppressed proton magnetic resonance spectroscopy.. Eight patients with acute stroke were studied serially in the acute phase, 1 week after, and 2-4 weeks after the onset of clinical symptoms. Ten healthy volunteers served as controls. A stimulated echo (STEAM) sequence was used for measurement of the brain metabolites in a volume of interest located within the infarcted area as visualized by magnetic resonance imaging. For quantification, the unsaturated water signal was used as the internal standard. Regional cerebral blood flow in the infarcted area was measured relative to a symmetrically located unaffected area by means of single-photon emission computed tomographic scanning, using 99mTc-labeled d,l-hexamethylenepropyleneamine oxime as the flow tracer.. Relative regional cerebral blood flow was considerably reduced in the infarcted area in the acute phase. After 1 week, hyperemia was seen in all but one patient. The N-acetylaspartate content was significantly reduced, with the loss appearing to occur between 6 and 24 hours after the stroke incident. The reduction in N-acetylaspartate content was greater in the central part than in the peripheral part of the infarcted area. Creatine and phosphocreatine were also reduced in the infarcted area, whereas no significant change was seen in the choline content.. Assuming that N-acetylaspartate content reflects neuronal survival or loss, our results may suggest that treatment procedures with restoration of blood flow to severely ischemic areas should be initiated within the first 6 hours after stroke onset.

Topics: Acute Disease; Adult; Aged; Aged, 80 and over; Aspartic Acid; Brain Chemistry; Cerebrovascular Circulation; Cerebrovascular Disorders; Choline; Creatine; Humans; Magnetic Resonance Imaging; Middle Aged; Phosphocreatine; Time Factors; Tissue Distribution

To determine the possible application of exogenous phosphocreatine (ePC) to protect the ischemic myocardium from reperfusion abnormalities in cardiac rhythm, the antiarrhythmic and antifibrillatory activities of the agent were studied in an acute myocardial ischemia model and reperfusion-induced cardiac damage. It was shown that ePC produced a pronounced antifibrillatory effect in acute coronary occlusion and subsequent reperfusion. The agent substantially increased the threshold of electric ventricular fibrillation and the frequency of spontaneous defibrillation. The highest activity was shown by ePC in ischemic myocardial reperfusion. The agent suppressed both rapid inward Na+ current and slow inward Ca2+ current. The effects of ePC on transmembrane ion currents suggest that the agent has a unique electrophysiological mechanism of action involving the properties of Classes I and IV antiarrhythmics, making ePC promising in clinical application in patients with impaired conduction and automatism.

Topics: Acute Disease; Animals; Arrhythmias, Cardiac; Cats; Coronary Disease; Myocardial Reperfusion Injury; Phosphocreatine

In acute and subacute hydrocephalus periventricular oedema is most prominent. At these stages of hydrocephalus, the free water content is increased and the bound water content, to the contrary, significantly decreased in the periventricular white matter. The bioenergetic state is also altered. In the chronic stage the ratio of free-to-bound water content returns to a level near the control value, leading to a decrease of periventricular oedema by formation of alternative pathways of CSF absorption. The bioenergetic state was slightly altered at this stage.

Topics: Acute Disease; Animals; Body Water; Brain; Chronic Disease; Dogs; Energy Metabolism; Hydrocephalus; Phosphates; Phosphocreatine

The effects of palmitate on mechanical failure of ischemic hearts were studied in acutely (48-hour) and chronically (6-week) streptozotocin diabetic rats. Coronary flow was reduced by 50% in isolated working hearts perfused at a 15 cm H2O preload and 100 mm Hg afterload by the one-way ball valve model of ischemia. Peak systolic pressure (PSP) and cardiac output (CO) decreased 40% by 4 minutes in control hearts perfused with 11 mM glucose and paced at 280 beats/min, compared with 50% in hearts from acutely diabetic rats. Addition of 1.2 mM palmitate to the perfusate accelerated failure rates, with PSP and CO decreasing 65% and 80% by 4 minutes in control and acutely diabetic rat hearts, respectively. In chronically diabetic rats, mechanical function could not be maintained in palmitate-perfused hearts paced at 280 beats/min, even in the absence of ischemia. If these hearts were paced at 250 beats/min and subjected to ischemia, PSP and CO decreased 90% by 4 minutes, regardless of whether palmitate was added to the perfusate. Under these conditions, PSP decreased less than 10% by 4 minutes in both palmitate- or glucose-perfused control hearts. Etomoxir (10(-9) M), a carnitine palmitoyltransferase I inhibitor, markedly decreased the rate of mechanical failure in both acutely and chronically diabetic rat hearts, in the presence and absence of palmitate. The beneficial effect of Etomoxir on mechanical function did not occur as a result of a decrease in either myocardial long chain acyl-coenzyme A or long chain acylcarnitine levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acute Disease; Acyl Coenzyme A; Acyltransferases; Animals; Carnitine O-Palmitoyltransferase; Chronic Disease; Coronary Disease; Diabetes Mellitus, Experimental; Epoxy Compounds; Fatty Acids; Heart; In Vitro Techniques; Male; Myocardium; Phosphocreatine; Rats; Rats, Inbred Strains; Streptozocin; Thiourea

The effect of phosphocreatine and phosphocreatinine disodium salts on excitation conduction in acute myocardial ischemia was investigated, using repeated short-term ischemia exposures of the isolated rabbit ventricular septum as a model. Considerable improvement of excitation conduction through ischemized myocardium, seen after the administration of phosphocreatine and phosphocreatinine salts, was shown to be associated with Na+ added to the perfusion medium. Phosphocreatine and phosphocreatinine effects on excitation conduction time and the septal force in control perfusion were related to both the addition of Na+ and the binding of Ca2+ by these agents in the perfusion medium.

Topics: Acute Disease; Animals; Arrhythmias, Cardiac; Calcium; Coronary Disease; Culture Media; Electric Stimulation; Heart Conduction System; In Vitro Techniques; Male; Phosphocreatine; Rabbits; Sodium

Using isotope-labeled microspheres (diameter 15 microns) it was shown that phosphocreatine at a dose of 300 mg/kg does not affect the myocardial blood flow in the ischemic zone during acute occlusion (5 min) of the left anterior descending coronary artery (LAD) in dogs. Intravenous administration of NaCl hypertonic solution which contained the same amount of Na+ as 300 mg/kg of phosphocreatinine disodium salt prevented the development of ventricular fibrillation during acute LAD occlusion in dogs. Under these conditions excitation conduction velocity significantly increased. Experiments in isolated intraventricular rabbit septum have showed that the addition of phosphocreatine or phosphocreatinine to the perfusion medium at a concentration of 10 mmole/liter increased excitation conduction velocity in ischemic myocardium. However, when changes in perfusate Na+ and Ca2+ concentration produced by addition of phosphocreatine or phosphocreatinine were compensated, these compounds do not affect excitation conduction velocity. On the other hand, the alterations similar to those produced by the addition of phosphocreatine or phosphocreatinine led to the same increase of excitation conduction velocity. The results obtained indicate an important role of the changes of blood plasma ionic composition on intravenous administration of phosphocreatine in electrophysiological and antiarrhythmic effects of this substance during acute myocardial ischemia.

Topics: Acute Disease; Animals; Blood Pressure; Calcium; Coronary Circulation; Coronary Disease; Coronary Vessels; Dogs; Heart; Heart Rate; In Vitro Techniques; Myocardial Contraction; Phosphocreatine; Reference Values; Sodium

Topics: Acute Disease; Aged; Female; Humans; Hypokalemia; Middle Aged; Phosphocreatine; Potassium; Rhabdomyolysis

Quadriceps femoris muscle needle biopsies were performed in ten patients with chronic obstructive pulmonary disease and acute respiratory failure and in ten age- and sex-matched healthy control subjects. The main indices of skeletal muscle cell energy metabolism, intracellular acid-base equilibrium and lactate metabolism were evaluated. Reduced ATP and phosphocreatine content, intracellular acidosis related to hypercapnia, increased muscle lactate without alterations of the muscle lactate concentration gradient were observed in the skeletal muscle of the hypercapnic-hypoxemic COPD patients studied, in which group no correlation was found between hypoxia and energy or lactate metabolism parameters. These results suggest that an overall derangement of cell energy metabolism and acid-base equilibrium is present in severely hypercapnic-hypoxemic chronic obstructive pulmonary disease and that in this condition skeletal muscle seems to metabolize anaerobically-even though, in addition to hypoxia, other factors interfering with both cell energy and lactate metabolism are likely to be present.

Topics: Acid-Base Equilibrium; Acute Disease; Adenosine Triphosphate; Aged; Energy Metabolism; Female; Humans; Hypercapnia; Hypoxia; Lactates; Lactic Acid; Lung Diseases, Obstructive; Male; Middle Aged; Muscles; Phosphocreatine; Respiratory Insufficiency

Topics: Acute Disease; Animals; Chronic Disease; Diastole; Energy Metabolism; Guinea Pigs; In Vitro Techniques; Myocardial Contraction; Myocardium; Phosphocreatine; Rats

Absence of a Major Arrhythmogenic Role for Cyclic AMP. Journal of Molecular and Cellular Cardiology (1986) 18, 375-387. We examined the mechanism whereby beta-adrenoceptor antagonism exerts an antiarrhythmic effect in early myocardial ischaemia. Ligation of the anterior descending coronary artery in the anaesthetized open-chest pig resulted in severe transmural anteroseptal ischaemia. Blood flow in the mid-ischaemic zone 20 min after ligation was decreased to 5.7 +/- 0.7% of the preligation control value. Epicardial ST-segment deflections of 6.7 +/- 0.4 mV were recorded over this zone. A distinct phase of ventricular arrhythmias was evident about 10 to 30 min after ligation. A high incidence of ventricular fibrillation (14/16 pigs) was associated with a circumstantial increase in levels of cyclic AMP in ischaemic tissue. Twenty minute values were: 1.10 +/- 0.06, P less than 0.05 v. the non-ischaemic tissue level of 0.86 +/- 0.05 nmol/g. Propranolol 3 mg/kg IV, metoprolol 20 mg/kg IV or sotalol 10 mg/kg IV were given between 30 min prior to and 10 min after ligation. Adequate beta-adrenoceptor antagonism by each agent could be proven. Metoprolol decreased the incidence of ventricular fibrillation (2/13, P less than 0.0005 v. control group), while propranolol or sotalol did not. All three beta-antagonists decreased tissue levels of cyclic AMP prior to ligation. However, the temporary increase in ischaemic tissue after ligation could not be prevented. Furthermore, cyclic AMP in ischaemic tissue 20 min after ligation was higher in the metoprolol group than in the propranolol or sotalol group (0.94 +/- 0.04 v. 0.81 +/- 0.02 P less than 0.05, and 0.79 +/- 0.03 nmol/g P less than 0.01, respectively). Blood flow in the mid-ischaemic zone of the metoprolol group was increased to 8.6 +/- 0.6% of preligation control value (P less than 0.0001 v. control group). In contrast, blood flow in the mid-ischaemic zone of the propranolol or sotalol group was decreased. Metoprolol also reduced epicardial ST-segment deflections over the mid-ischaemic zone to 3.5 +/- 0.2 mV (P less than 0.0001 v. control group). ST-segment deflections in the propranolol group were increased. The mechanism whereby metoprolol prevented ventricular fibrillation may be explained by a decrease in the severity of ischaemia but not in terms of changes of tissue levels of cyclic AMP.

Topics: Acute Disease; Adenosine Triphosphate; Animals; Arrhythmias, Cardiac; Blood Pressure; Coronary Circulation; Coronary Disease; Cyclic AMP; Electrocardiography; Female; Heart Rate; Lactates; Male; Metoprolol; Phosphates; Phosphocreatine; Propranolol; Sotalol; Swine; Time Factors; Ventricular Fibrillation

The association between phosphocreatine's antifibrillatory action and its effect on the excitement propagation processes in the ischemic area was investigated under acute coronary arterial occlusion in dogs. Ischemia considerably reduced the amplitude, and increased the duration and time of onset, in local electrograms, and provoked cardiac fibrillation at the time of occlusion or during the recovery of coronary flow. A single intravenous injection of 300 mg/kg phosphocreatine eliminated cardiac fibrillation and largely prevented electrographic changes in the ischemized area. Phosphocreatinine, phosphocreatine's structural analogue, produced a similar effect. It is suggested that antiarrhythmic action of phosphocreatine and phosphocreatinine is mediated by their membrane effects.

Topics: Acute Disease; Animals; Anti-Arrhythmia Agents; Coronary Disease; Dogs; Drug Evaluation, Preclinical; Heart Conduction System; Kinetics; Phosphocreatine; Ventricular Fibrillation

A dog model was used to measure the hemodynamic changes occurring during acute pancreatitis induced by intraductal injection of fresh trypsin-bile-blood mixture. Pancreatic blood flow was measured with 15-micrometer radioactive microspheres. Measurements of pancreatic adenosine triphosphate (ATP) and creatine phosphate (CP) were made under normal conditions and during acute hemorrhagic pancreatitis. Basal ATP and CP concentrations were 5.82 +/- 0.25 and 5.30 +/- 0.31 mmol/g wet tissue, respectively. Hemorrhagic pancreatitis was characterized by a severe reduction in pancreatic blood flow, followed by a 45% fall of ATP and a 70% lowering of CP. These results suggest that inadequate pancreatic tissue perfusion during acute pancreatitis results in a marked depletion of high-energy phosphate stores. We suspect this energy depletion reflects the progression of the disease from edematous to hemorrhagic pancreatitis and causes irreversible damage of pancreatic tissue.

Topics: Acute Disease; Adenosine Triphosphate; Animals; Dogs; Hemodynamics; Hemorrhage; Pancreas; Pancreatitis; Phosphocreatine; Regional Blood Flow

We analyzed brain tissue for adenosine and its metabolites, inosine and hypoxanthine, in rats during acute (30 s) hypoxia and during sustained (5 min) hypoxia and hypocarbia. Within 30 s of the onset of hypoxia, adenosine levels were increased from 0.34 +/- 0.08 (SE) to 1.65 +/- 0.33 nmol/g (P less than 0.005), paralleling temporally the changes in cerebral blood flow. During sustained hypoxia and hypocarbia, brain tissue was sampled by a fast (freeze-blow) or slow (in situ) freezing method. With the freeze-blow technique, adenosine concentrations remained stable between arterial partial pressure of O2 (PaO2) greater than 200 and 100 mmHg, doubled at PaO2 = 50 mmHg, and increased sevenfold (P less than 0.005) when PaO2 reached 30 mmHg. No increases in adenosine or its metabolites were noted with the in situ technique. During hypocarbia (arterial CO2 partial pressure less than 20 mmHg), adenosine concentrations increased with both sampling techniques. Freezing times in brain were measured during in situ freezing and were increased during hypoxia and decreased during hypocarbia. In conclusion, 1) adenosine concentrations in brain are increased during hypoxia, and 2) the in situ technique in rat does not appear to be optimal for sampling brain tissue for subsequent measurement of adenosine under conditions where cerebral blood flow is increased.

Topics: Acute Disease; Adenine Nucleotides; Adenosine; Animals; Arteries; Blood; Brain Chemistry; Carbon Dioxide; Freezing; Hypoxia, Brain; Lactates; Lactic Acid; Oxygen; Partial Pressure; Phosphocreatine; Rats; Time Factors

Topics: Acute Disease; Adenosine Triphosphate; Animals; Coronary Disease; Glycogen; Lactates; Myocardium; Osmolar Concentration; Perfusion; Phosphocreatine; Potassium; Sodium; Swine; Water

The glycolytic substrate utilization and energy consumption of hemispheres of adult mice were studied by converting the heads into a closed system by decapitation. It was concluded that progressive insufficiency of renal function is paralleled by an increase in brain permeability for glucose and a progressive reduction in brain energy metabolism.

Topics: Acute Disease; Adenosine Triphosphate; Animals; Anuria; Blood Glucose; Brain; Cell Membrane Permeability; Energy Metabolism; Glycogen; Glycolysis; Male; Mice; Oxygen Consumption; Phosphocreatine; Urea

1. The concentration of metabolites in intercostal and quadriceps muscle, and pulmonary function, were studied in twelve patients with chronic obstructive lung disease and acute respiratory failure before, during and after standardized treatment at an intensive care unit. The findings were compared with those obtained in hospitalized patients of comparable age with non-pulmonary diseases. 2. On admission, when the patients had marked hypoxaemia, hypercapnia and acidosis, the concentrations of ATP and creatine phosphate were low in both intercostal and quadriceps muscle, particularly the latter. The lactate concentration was increased in relation to control values but glycogen did not differ significantly. 3. In response to therapy, the Pa,CO2 and the patient's acidosis decreased, the vital capacity increased and lung mechanics improved along with the clinical condition. At the same time there were significant increases in the concentrations of ATP, creatine phosphate and glycogen in intercostal and quadriceps muscles, to values similar to, and for glycogen in excess of, those found in control subjects. Lactate concentration fell significantly during treatment. 4. In view of the low initial muscle concentrations of ATP and creatine phosphate in the patients, it is suggested that dysfunction of the respiratory muscles may be an important component of respiratory failure. Moreover, the concentration of energy-rich compounds in muscle rose significantly as the patients responded to treatment, which emphasizes the importance of adequate nutritional therapy in this disorder.

Topics: Acute Disease; Adenosine Triphosphate; Aged; Chronic Disease; Female; Glycogen; Humans; Intercostal Muscles; Lactates; Lung Diseases, Obstructive; Male; Middle Aged; Muscles; Phosphocreatine; Respiratory Function Tests; Respiratory Insufficiency

Subcellular fractions in hearts from rats with severe acute uremia (24 hours after total nephrectomy) and moderate chronic uremia (2 weeks after five sixths nephrectomy) were studied and compared with preparations from acute and chronic sham-operated rats, respectively. Calcium- and magnesium-sensitive actomyosin adenosine triphosphatase (ATPase) activities were normal in both groups. Acute uremia was associated with a significant depression of sarcolemmal Na+,K+ ATPase activity. Calcium transport by fragmented sarcoplasmic reticulum was also depressed in the presence and absence of oxalate in acute uremia. Mitochondrial calcium transport and adenosine triphosphate (ATP) and creatine phosphate (CP) concentrations were normal in these animals. Chronic uremic animals showed no abnormal subcellular mechanisms. These data suggest a direct effect of acute uremia on some membrane functions in myocardial cells. The discrepancies observed between acute and chronic uremic groups may be due to a different degree of uremic state. The observation of depressed calcium transport by fragmented sarcoplasmic reticulum (FSR) in acute uremic hearts which were previously shown to have increased contractile reserve suggests that studies of calcium transport in FSR may not always truly reflect the contractile capacity of the heart.

Topics: Actomyosin; Acute Disease; Adenosine Triphosphatases; Adenosine Triphosphate; Animals; Biological Transport, Active; Calcium; Chronic Disease; Male; Mitochondria, Muscle; Myocardial Contraction; Myocardium; Phosphocreatine; Potassium; Rats; Sarcoplasmic Reticulum; Sodium; Uremia

The extent to which changes in tissue energy metabolism correspond to the severity of a hemorrhagic shock condition has been studied. In cats, 50% of the blood volume was withdrawn within 10 min, resulting in a fatal outcome within 3h (range from 45 min to 3 h). Skeletal muscle and blood samples were taken prior to the hemorrhagic and in the agonal phase or after 2 h in compensated bled animals. Tissue levels of ATP, CrP, G-6-P, lactate and glucose as well as blood levels of glucose, lactate and pyruvate were determined enzymatically. The results showed no depletion of phosphagen levels in the agonal phase, while glycolytic metabolites, lactate in particular, demonstrated a close correlation to circulatory deterioration and imminent death.

Topics: Acute Disease; Adenosine Triphosphate; Animals; Blood Glucose; Cats; Female; Glucose; Glucosephosphates; Lactates; Muscles; Phosphocreatine; Pyruvates; Shock, Hemorrhagic

Acute myocardical ischemia was produced by ligating the midlevel left anterior descending coronary artery for 17 min in anesthetized dogs. Epicardial electrocardiograms were recorded from 15 sites surrounding the area of left anterior descending coronary artery ligation with a smooth tip, rounded epicardial electrode. Sites of ST segment elevation and isoelectric sites within the grossly ischemic portion of the left ventricle were needle biopsied to obtain tissue samples of less than 6 mg wet weight to assess myocardial metabolism at these precise sites. Epicardial areas of ST segment elevation had marked lactate accumulation and high energy phosphate depletion. Isoelectric sites were areas of either no lactate accumulation or mild lactate accumulation and high energy phosphate concentrations that were greater than those found at site of ST segment elevation. Thus, the data obtained indicate that epicardial sites of ST segment elevation are locations of profound anaerobic metabolism and of both epicardial and endocardial ischemia.

Topics: Acute Disease; Adenosine Triphosphate; Coronary Circulation; Coronary Disease; Electrocardiography; Hypoxia; Lactates; Membrane Potentials; Myocardium; Phosphocreatine

Topics: Acute Disease; Adenosine Triphosphate; Animals; Aspartate Aminotransferases; Biopsy, Needle; Creatine Kinase; Female; Gait; Glucose; Glucosephosphates; Horse Diseases; Horses; Lactates; Male; Methods; Microscopy, Electron; Muscles; Myoglobinuria; Phosphocreatine; Time Factors

Topics: Acute Disease; Adenine Nucleotides; Adenosine Diphosphate; Adenosine Monophosphate; Adenosine Triphosphate; Ammonia; Animals; Bicarbonates; Blood; Body Temperature; Brain; Carbon Dioxide; Citric Acid Cycle; Glucose; Hydrogen-Ion Concentration; Hypercapnia; Ketoglutaric Acids; Lactates; Malates; Male; Nitrous Oxide; Phosphocreatine; Pyruvates; Rats; Temperature; Time Factors

Topics: Acute Disease; Adaptation, Physiological; Animals; Aortic Coarctation; Cathepsins; Deoxyribonucleases; Heart; Heart Function Tests; Male; Myocardium; Phosphocreatine; Phosphoric Monoester Hydrolases; Physical Exertion; Rats; Ribonucleases; Time Factors

Topics: Acute Disease; Adenosine Diphosphate; Adenosine Monophosphate; Adenosine Triphosphate; Animals; Coronary Vessels; Dogs; Glycogen; Glycolysis; Heart Ventricles; Mitochondria, Muscle; Myocardial Infarction; Myocardium; Oxidative Phosphorylation; Oxygen Consumption; Phosphocreatine

Topics: Acute Disease; Adenine Nucleotides; Aerobiosis; Anaerobiosis; Animals; Coronary Disease; Coronary Vessels; Disease Models, Animal; Dogs; Fatty Acids; Glucose; Glycolysis; Hydrogen-Ion Concentration; Lactates; Mitochondria, Muscle; Models, Biological; Myocardial Infarction; Myocardium; Phosphocreatine

Topics: Acute Disease; Adenosine Triphosphate; Animals; Coronary Disease; Coronary Vessels; Disease Models, Animal; Dogs; Lactates; Myocardial Infarction; Myocardium; Phosphocreatine; Time Factors

Topics: Acute Disease; Adenine Nucleotides; Adenosine Triphosphate; Alanine Transaminase; Animals; Aspartate Aminotransferases; Cerebellum; Citrates; Fructosephosphates; Gluconates; Glucose; Glucosephosphates; Glycogen; Hypoxia, Brain; Ischemic Attack, Transient; Ketoglutaric Acids; Lactates; Malates; Male; Medulla Oblongata; Mesencephalon; Mice; Oxygen Consumption; Parietal Lobe; Phosphocreatine; Pons; Pyruvates; Respiratory Insufficiency

Topics: Acute Disease; Animals; Brain Chemistry; Carbon Dioxide; Chronic Disease; Glutamates; Hydrogen-Ion Concentration; Hypercapnia; Ketoglutaric Acids; Lactates; Male; Phosphocreatine; Pyruvates; Rats; Time Factors

Topics: Acute Disease; Adenosine Triphosphate; Animals; Blood Glucose; Brain; Carbohydrate Metabolism; Carbon Monoxide Poisoning; Chronic Disease; Female; Glycogen; Lactates; Phosphocreatine; Pyruvates; Rats