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

Isolated working rat hearts were made ischemic by introducing a one-way aortic ball valve. After the ischemic period the hearts were perfused in a retrograde non-working way for 30 min. Flow rates, glycogen, ATP, and creatine-phosphate went down during the time of ischemia, whereas tissue lactate accumulated. For shorter periods of ischemia these values were normalized but after 30 min of ischemia the hearts seemed to be irreversibly damaged. There was a leakage of GOT, GPT, LDH, and CPK from all hearts when ischemic from 5 to 30 min. Different factors that might be of importance for the degree of ischemic injury were tested. The injury tended to be more severe at higher heart rates. Addition of adrenaline 10(-6)M resulted in excessive myocardial damage. A variation of pH from 7.1 to 7.7 did not alter the effects of the ischemic injury. One group of rats were injected with adrenaline for 8 weeks to simulate chronic stress. When hearts from these rats were made ischemic they were more prone to fail compared to controls. The failing hearts, on the other hand, had a lower leakage of enzymes, possibly due to a less severe myocardial damage. A high mechanical performance and a normal noradrenaline content of the hearts are key factors for the development of myocardial infarction, as indicated by this study.
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PMID:Factors of importance for the degree of ischemic injury in the isolated rat heart. 0 96

Changes in cerebral cortex concentrations of high-energy phosphates, glycolytic metabolites, citric acid cycle intermediates, associated amino acids, and ammonia, were studied after 5, 15 and 30 min of incomplete ischemia in rats anesthetized with 70% N2O or 150 mg.kg-1 of phenobartibal. Previous results have shown that with this type of ischemia (bilateral carotid artery occlusion combined with reduction in blood pressure to 50 mm Hg) cortical blood flow is reduced to below 10% of nitrous oxide values, whether animals are anesthetized with 70% N2O or 150 mg.kg-1 of phenobarbital. In animals under 70% N2O, changes in tissue concentrations of phosphocreatine, ATP, ADP and AMP were similar to those previously obtained in complete ischemia. However, some glucose remained in the tissue, and the lactate concentrations gradually rose to reach excessive values. Changes occuring in glycolytic and citric acid cycle intermediates were similar to those seen in complete ischemia but, after 30 min, there was some reduction in the pool size of amino acids. In those animals given phenobarbital and which lost all EEG activity during ischemia, changes in cerebral metabolites were virtually identical to those observed in nitrous oxide-anesthetized animals. However, some animals exposed to 5 or 15 min of ischemia had some remaining EEG activity. In these, cerebral energy state was significantly less deranged, and levels of glycogen, glucose and pyruvate were higher.
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PMID:Effects of phenobarbital in cerebral ischemia. Part I: cerebral energy metabolism during pronounced incomplete ischemia. 2 84

Restoration of blood flow after 15 or 45 min. of ischemia induced an immediate recovery of phosphocreatine level and adenylate energy charge whereas ATP and total adenine nucleotides remained significantly below their normal values. These results prove that oxidative phosphorylations are not impaired but that a pool of myocardial adenine nucleotides is lost during ischemia which cannot be restored shortly after reperfusion. The significance of energy charge as a regulatory parameter in the myocardium is discussed.
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PMID:[Biochemical effects of reperfusion after regional myocardial ischemia of different duration in the open chest dog]. 11 59

In vivo interstitial muscle pressures measured by wick catheter, tissue gas tensions measured by mass spectrometer, and glucose and high-energy phosphate metabolism measured fluorometrically were studied in the anterior tibial (AT) and vastus lateralis (VL) muscles of primate limbs during and following tourniquet ischemia (2.5 hours; 400 mm Hg) to elucidate postischemic edema and its metabolic consequences. During ischemia, interstitial pressure in the VL rose, while in the AT it decreased, but 24 hours later pressures in both experimental muscles were significantly greater than those in the controls. In both experimental muscles PO2 decreased significantly within 15 minutes of ischemia. PCO2 increased significantly in the AT at 30 minutes and at 75 minutes in the VL muscle. Twenty-four hours later only PO2 in the experimental AT was significantly different than its matched control. During ischemia glucose and phosphocreatine (CrP) decreased significantly, and G-6-P and lactate increased significantly in both muscles, but at 24 hours glucose levels were 25% lower and G-6-P 16.2% higher in the experimental AT and CrP 34% lower in the experimental VL. This study shows that there are significant acute and delayed alterations in primate muscle metabolism following tourniquet ischemia and suggests that these changes may be related to the anatomic location of the muscle studied and the type of trauma it has sustained.
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PMID:Effects of tourniquet ischemia and postischemic edema on muscle metabolism. 11 47

In Langendorff-perfused rat hearts, the perfusion pressure was reduced from 100 cm H2O to 20 cm H2O for 30 minutes to produce a model of global ischemia with a residual oxygen uptake. The release of lactate dehydrogenase (LDH) and the occurrence of ventricular arrhythmias during reperfusion were dependent on the substrate. Glucose-perfused hearts had the highest rates of glycolytic ATP production (2.5 mumol/g per min) during ischemia with normal contents of tissue cyclic adenosine 3',5'-monophosphate (cAMP) and, during reperfusion, the release of LDH was lowest and severe ventricular arrhythmias did not occur. In pyruvate-perfused hearts, glycolysis was inhibited during ischemia, the rate of production of glycolytic ATP was only 0.5 mumol/g per min. and tissue cAMP doubled; during reperfusion, LDH release was 14-fold higher and ventricular arrhythmias were more severe. Total tissue contents of ATP and phosphocreatine were similar in glucose- and in pyruvate-perfused hearts. In hearts perfused with acetate, there was virtually no glycolytic ATP synthesized during the last 5 minutes of ischemia and cAMP increased further. Acetate- and palmitate-perfused hearts showed greatest release of LDH and had severest arrhythmias during reperfusion, suggesting that it was the metabolic and not the detergent effects of palmitate that were operating. Lipolysis was not a major factor in the cause of reperfusion LDH release. A role of glycolytic ATP in the maintenance of membrane integrity is postulated.
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PMID:Effects of substrates on tissue metabolic changes in the isolated rat heart during underperfusion and on release of lactate dehydrogenase and arrhythmias during reperfusion. 20 59

The effects of ligation of both common carotid arteries in the gerbil on the levels of PGF2 alpha, TXB2, HETE and of energy metabolites in brain cortex, have been investigated. Also, in the same experimental conditions the changes of cyclic AMP in brain cortex, cerebellum, striatum and hippocampus have been monitored. ATP, glycogen, glucose and phosphocreatine decrease whereas, lactate and cyclic AMP are enhanced in the ischemic brain, as previously reported. In contrast, levels of arachidonic acid metabolites are not modified. During ischemia following decapitation, instead, PGF2 alpha, and TXB2, show considerable increase.
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PMID:PGF2 alpha, thromboxane B2 and HETE levels in gerbil brain cortex after ligation of common carotid arteries and decapitation. 23 May 39

31P nuclear magnetic resonance (NMR) studies of creatine phosphokinase (CPK) kinetics using saturation transfer techniques are reported. The phosphocreatine (PCr) and adenosine triphosphate (ATP) levels in perfused hearts can be altered experimentally by stopping the flow of perusate (ischemia) to the heart for 35-min periods, followed by reperfusion to produce stable levels of performance. Utilization of energy by the heart was altered by administration of 25 mM potassium chloride (KCl) in the perfusate, which arrests contraction of the myocardium. Compared with control heart studies, the unidirectional rates measured during ischemia and KCl arrest are altered. The rates observed in the control experiments indicate that the CPK system is not in a steady state. This apparent deviation from steady-state conditions is ascribed to the existence of intracellular compartmentation of ATP.
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PMID:Adenosine triphosphate compartmentation in living hearts: a phosphorus nuclear magnetic resonance saturation transfer study. 47 74

In rats, cerebral perfusion pressure were altered abruptly by aortic transection to determine the production by ischemic brain of adenosine and its metabolites, inosine and hypoxanthine. Brain samples were obtained after 0, 5, 10, 15, 30, and 60 seconds of ischemia. Also measured were ATP, ADP, AMP, phosphocreatine (PCr), lactate, and pyruvate. Blood pressure was monitored continuously, and arterial PO2, PCO2, and pH were measured just prior to induction of ischemia. Adenosine was elevated t 2.30 +/- 0.31 (SE) nmol/g at 5 seconds from a control value of 0.96 +/- 0.07. A significant elevation of adenosine continued to 60 seconds (5.50 +/- 1.24). Furthermore, inosine showed a progressive upward trend during the entire 60 seconds of ischemia, whereas no change in hypoxanthine occurred between the moment of transection (31.81 +/- 2.01 nmol/g) and 60 seconds of ischemia (34.72 +/- 2.93). PCr decreased by 1.24 mumol/g within the first 5 seconds. After the onset of hypotension, significant changes did not occur in AMP and ADP until 30 seconds, and in ATP and pyruvate until 60 seconds after aortic transection; lactate was elevated by 10 seconds. The rapid rise of cerebral adenosine within 5 seconds after the onset of ischemia supports a role for adenosine in the regulation of cerebral blood flow.
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PMID:Brain adenosine production in the rat during 60 seconds of ischemia. 47 71

The effect of 1.5 to 2.5 h tourniquet ischemia on energy metabolism of the quadriceps muscle was studied using percutaneous needle biopsy technique in sixteen patients operated on for an inveterated knee injury. During occlusion there was a moderate decrease in ATP with an increase in ADP and AMP. This change resulted in a decreased energy charge potential. At the same time phosphorylcreatine (PC) decreased markedly while creatine (Cr) increased giving a constant total creatine (TCr). An accumulation of lactate during occlusion with values up to 80 mmol/kg d.m. (dry muscle) was seen. A 15% reduction in glycogen was calculated. After release of the tourniquet the active phosphate concentration and the energy charge potential returned to basal levels within 5 min and most of the metabolites in the glycolytic sequence were also normalized. Muscle lactate content was normal after 30 min of intact circulation. The results suggest that longterm tourniquet ischemia induces marked changes in energy metabolism in skeletal muscle, but that the changes are rapidly and completely reversible with restoration of blood flow.
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PMID:The effect of long-term arterial occlusion on energy metabolism of the human quadriceps muscle. 52 75

The effect of pretreatment with ouabain (40 microgram/kg, i.v.) on myocardial metabolic and contractile responses to regional ischemia induced by coronary artery ligation was studied in the canine left ventricle. In control dogs, ischemia increased activity of phosphorylase a and the levels of glucose-6-phosphate and lactate, and decreased the levels of glycogen and phosphocreatine, without affecting the levels of adenosine triphosphate, adenosine diphosphate, and adenosine monophosphate (AMP). Ouabain increased the activity of phosphorylase a. In ouabain-treated dogs, ischemia did not further increase the phosphorylase a activity but it increased the epicardial AMP level. Other metabolic responses to ischemia in ouabain-treated dogs were similar to those in control dogs. In control dogs, myocardial contractile force decreased by about 10% after ischemia, but blood pressure and heart rate remained unchanged. Ouabain increased contractile force by about 32%. In ouabain-treated dogs, ischemia decreased contractile force by about 54% without affecting blood pressure and heart rate. It is concluded that ouabain increases the activity of the myocardial phosphorylase a and that the inotropic action of ouabain can be nullified by coronary artery ligation.
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PMID:Effect of ouabain on myocardial metabolic and contractile responses to coronary ligation. 61 33


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