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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Metabolite levels were measured in seven brain regions in cats after 15 or 30 minutes of a severe ischemic insult and after a 90-minute period of recirculation following 15 or 30 minutes of ischemia. Brain levels of phosphocreatine were depleted after a 15- or 30-minute insult, and lactate levels were extremely high at both times. The adenosine triphosphate (ATP) content in many brain areas and the presence of microregions of low reduced nicotinamine-adenine dinucleotide in the brains of the animals that had 15 minutes of ischemia suggested that the ischemia, though severe, was not complete. Recirculation following a 15-minute insult restored brain levels of ATP and phosphocreatine to 70 to 100% of control values in all regions analyzed. In contrast, metabolic recovery from a 30-minute insult was regionally heterogeneous. Thus, there was persistent depression of ATP and phosphocreatine and elevation of lactate, which was localized in discrete cortical foci near the longitudinal midline. The factors governing the localization of metabolic failure must have become manifest during the recirculation period since the ischemic insult itself caused similar metabolic perturbations in all cortical regions.
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PMID:Diffuse cerebral ischemia in the cat: II. Regional metabolites during severe ischemia and recirculation. 67 15

The present study, which concerns the rate of changes in the cerebral cortex concentrations of phosphocreatine (PCr), ATP, ADP, AMP, lactate and pyruvate during complete ischemia, had the objective of finding out whether or not phenobarbital retards depletion of tissue energy reserves during ischemia. Ischemia was induced for periods of 10 s to 10 min in animals maintained on 70% N2O or given 150 mg.kg-1 of phenobarbital. The results showed that the barbiturate anaesthesia delayed utilization of ATP during the first 2 min. However, after 5 min of ischemia PCr and ATP concentrations, as well as the calculated adenylate energy charge, were identical in animals anaesthetized with nitrous oxide and phenobarbital. Thus, phenobarbital induces a very moderate delay in the depletion of cerebral energy reserves that occurs during complete ischemia. The results obtained after 5-20 s of ischemia allowed calculation of energy (approximately P) utilization according to Lowry et al. (1964). The closed system method gave values for approximately P utilization which were not far from those obtained by CMRo2 measurements. However, with normal values for metabolic rate (70% N2O) valid estimates are obtained only with very short ischemic periods (5-10 s) and, with such short periods, the oxygen content of the tissue may introduce an error.
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PMID:Influence of phenobarbital on changes in the metabolites of the energy reserve of the cerebral cortex following complete ischemia. 71 81

To determine the relationship between brain energy metabolites and neurologic status after ischemia-hypoxia, we measured cortical tissue levels of adenosine triphosphate (ATP), phosphocreatine, and lactate. Rats with permanent unilateral carotid occlusion were exposed to 5, 10, and 15 min of hypoxic atmosphere (FIO2 0.048) and, to examine metabolic restitution, 60 min after recovery in rats exposed to the same hypoxic mixture for 15 min. At 5 and 10 min of hypoxia, there were significant reductions in phosphocreatinine and elevations in tissue lactate, but only after 15 min of hypoxia, did ATP levels significantly decrease. By 60 min after recovery, phosphocreatinine values returned to the normal range, ATP values to 15% less than normal, and tissue lactate toward normal. In parallel survival studies, neurological status was examined following hypoxic exposure (PaO2 18 to 19 torr) for 5 an 10 min. Evidence for neurological injury in the form of posthypoxic seizures occurred at a point in time preceding significant changes in brain tissue ATP level. Since injury occurs prior to ATP reduction, changes in brain tissue ATP level may not be an appropirate endpoint for determining brain tissue injury in hypoxia.
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PMID:Cerebral energy metabolite levels and survival following exposure to low inspired oxygen concentration. 72 89

The effects of atrial pacing on tissue metabolite levels known to be sensitive to ischemia were examined. Anesthetized dogs were thoracotomized and a pacing electrode was sutured to the right atrium. Pacing at rates of 200 or 250 beats/min (10 animals per group) was performed for 15 min after base-line hemodynamic data had been obtained. At the end of the pacing period, a transmural biopsy was taken, frozen in liquid nitrogen, and sectioned into subepicardial, midmyocardial, and subendocardial layers. ATP, phosphocreatine, lactate, and glycogen were extracted and analyzed. Significant (P less than 0.001) transmural gradients of each of these metabolites existed in the control group. Pacing had no significant (P greater than 0.2) effect on any metabolite from layer to layer at 200 or 250 beats/min. However, indices of heart work (i.e., contractility (dP/dt), stroke work, and stroke volume) demonstrated significant reductions (P less than 0.01) due to pacing, while circumflex artery blood flow increased more than twofold (P less than 0.001) at the highest rate. These data suggest that physiologic autoregulation occurred during pacing and protected the subendocardium from stress-induced ischemic insult.
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PMID:Transmural metabolic gradients in the normal dog left ventricle: effect of right atrial pacing. 88 64

Normal or elevated levels of ATP and phosphocreatine (PCr) were observed from the subepicardium to the subendocardium of the canine left ventricle after five and 20 minutes of left circumflex artery occlusion followed by 20 minutes of blood reflow. However, after two or four hours of occlusion, followed by reflow, ATP and PCr levels were markedly depressed, and a significant decreasing decreasing subepicardial to subendocardial gradient appeared, suggestive of inhibition of oxidative metabolism during extended periods of ischemia but not during short periods of ischemia.
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PMID:The effects of coronary artery ligation on transmural high-energy phosphates following 20 minutes of blood reflow. 103 12

The extent of cellular metabolic deterioration and its reversibility was studied on human skeletal muscle needle biopsies during operations in bloodless field. The tissue levels of high energy phosphates and glycolytic metabolites were analyzed after various times of tourniquet ischemia and compared to contralateral control extremity levels. In the ischemic extremity the phosphocreatine (CrP) levels decreased by 40% within 30-60 min and after 60-90 min a 60% reduction was found. No significant ATP changes occurred. Lactate levels increased by 225% after 30-60 min and by 300% after 60-90 min. The glucose and G-6-P levels increased slightly and indicated glycogenolysis. The rate of the metabolic changes decreased with ischemia time. In the control leg no significant metabolic changes could be seen. After the release of the tourniquet there was a rapid restoration of the phosphagen content and clearance of lactate in the ischemic leg. Near control levels of these substances were seen already after 5 min. The present results show that clinical tourniquet ischemia of up to 90 min duration produces less pronounced metabolic alterations than those seen in working muscle.
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PMID:Human skeletal muscle energy metabolism during and after complete tourniquet ischemia. 114 14

Adult rhesus monkeys were subjected to complete cerebral ischemia for one hour and subsequent recirculation for up to 24 h. Animals with signs of functional recovery (e.g. spontaneous EEG activity) exhibited a partial replenishment of cellular energy sources (ATP, phosphocreatine) and a progressive normalization of cerebral lactate levels. Glucose and pyruvate concentrations showed a transient increase over control values during the early stages of postischemic recirculation. Monkeys without functional recovery lacked a significant resynthesis of energy-rich compounds; adenine nucleotides continued to decrease and lactate concentrations were higher than in animals subjected to ischemia without recirculation. Cerebral polysome profiles remained unaltered during the ischemic period but in all animals a marked disaggregation of polyribosomes with a concomitant increase in ribosomal subunits occurred after the onset of recirculation. In monkeys with indications of functional recovery these changes were reversible but a normal polysome profile was only observed after 24 h of recirculation. The results obtained indicate a postischemic depression of protein synthesis due to an inhibition of peptide chain initiation. After recirculation of the brain for 3-6 h there was evidence for an induction of enzymes involved in polyamine synthesis (ornithine decarboxylase and S-adenosylmethionine decarboxylase). No changes in the activity of these enzymes were observed at the end of the ischemic period, indicating that during complete cerebral ischemia not only the synthesis but also the catabolism of proteins is inhibited.
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PMID:Resuscitation of the monkey brain after one hour complete ischemia. III. Indications of metabolic recovery. 115 69

The ampullar endolymphatic potential (AEP) was studied in the guinea pig during ischemia and asphyxia and following systemic application of ethacrynic acid. In addition the specialized and nonspecialized portions of the ampullar wall were analyzed for ATP and P-creatine at different conditions of metabolic interference. Under control conditions the AEP amounted to + 4.6 +/- 1.2 mV. In both types of hypoxia the decline of the AEP proceeded on a much slower time scale than that of the cochlear endolymphatic potential (CEP), and the maximum negativity reached was considerably less. Quantitative analysis of both types of ampullar wall tissue indicated a much slower decline in hypoxia of ATP levels than in the stria vascularis. Changes in P-creatine levels were considerably more rapid. The AEP became reduced and changed polarity also by intoxication with ethacrynic acid (EA), but higher dosages (above 70 mg/kg) were necessary than for effects upon the CEP and much longer time periods were required for attainment of maximum negativity. The maximum negativity of the AEP was significantly greater at a dosage of 100 mg/kg of EA than during ischemia. At the point of maximum depression of the AEP P-creatine levels in both types of ampullar tissue were unchanged, but ATP levels were significantly reduced in the specialized portions of ampullar wall.
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PMID:Effects of anoxia and ethacrynic acid upon ampullar endolymphatic potential and upon high energy phosphates in ampullar wall. 125 96

The effects of metabolic accumulation on myocardial metabolism during global heart oxygen deprivation were evaluated in a working in situ swine heart preparation with controlled total coronary blood flow. Myocardial oxygen consumption was depressed to a similar extent by either reducing total coronary flow 60 per cent (ischemia, low coronary perfusion) in 10 swine or by decreasing coronary perfusate PO2 to 30 mm. Hg at normal flows (hypoxemia, high coronary perfusion) in 13 swine. Compared with findings in 13 control hearts, ischemia significantly (p less than 0.05) decreased myocardial oxygen consumption (640 to 390 mumole per hour per gram), glucose uptake (185 to 16 mumole per hour per gram), and free fatty acid consumption (32 to 17 mumole per hour per gram). ttissue levels of glycogen, creatine phosphate, and adenosine triphosphate (tatp) were significantly reduced (p less than 0.005), and tissue lactate, adenosine diphosphate (ADP), and adenosine monophosphate (AMP) were increased (p less than 0.001). During hypoxemia, glucose uptake was increased (240 mumole per hour per gram) and free fatty acid consumption was somewhat less depressed (19 mumole per hour per gram). Creatine phosphate and ATP were higher than with ischemia (p less than 0.01), and lactate, ADP, and AMP accumulations were less (p less than 0.01). Thus, in the period immediately following myocardial oxygen deprivation, inadequate coronary perfusion caused greater metabolic buildup which inhibited myocardial substrate utilization and energy production. High coronary perfusion, even though the perfusate was unoxygenated, was associated with greater preservation of substrate utilization, higher levels of high-energy phosphates, less accumulation of metabolic products, and a longer survival. These data suggest a critical role of coronary perfusion in protecting myocardial metabolism in the immediate period following global heart hypoxia.
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PMID:Effects of coronary perfusion during myocardial hypoxia. Comparison of metabolic and hemodynamic events with global ischemia and hypoxemia. 126 57

Reperfusion of the heart 30 min. after ischemia causes slight recovery of contractility and content of macroergic compounds in the myocardium tissue. Recovery of perfusion by the hypercalcium medium (0.05 mol/l) improves metabolism of the myocardium 30 min after ischemia. However, further perfusion by solution with physiological content of Ca2+ is followed by the development of the myocardium contracture, essential decrease in extracellular concentration of ATP and phosphocreatine. An increase in the extracellular sodium concentration and addition of macroergic compounds (ATR, phosphocreatine) adenosine, when reperfusing the heart by hypocalcium solution, improve the postischemic state of the myocardium and protect it from injuries during the following recovery of physiological Ca2+ content in the extracellular medium.
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PMID:[A decrease in cardiac sensitivity after ischemia to a change in the extracellular concentration of calcium ions]. 128 84


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