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

Male Wistar rats were subjected to forebrain ischemia of 10 min duration by clamping both common carotid arteries and simultaneously lowering systemic blood pressure to 40 mm Hg by exsanguination. Recovery was achieved by removing the arterial clamps and reinfusing the blood. Cortical levels of high-energy phosphates and glycolytic substrates were determined enzymatically. Naftidrofuryl (10 or 20 mg/kg i.p.) or ketamine (5 mg/kg i.v.) were applied 30 min prior to the induction of ischemia. S(-)-Emopamil (4 mg/kg) or nimodipine (50 micrograms/kg) were administered by intravenous infusion over 30 min. Nimodipine and emopamil increased the blood glucose level and lowered preischemic blood pressure. Under control conditions, a tendency toward a higher cortical glucose level was observed in treated brains. Brain energy stores were exhausted after ischemia in control and treated animals to the same degree. Lactate levels, however, were higher in emopamil-treated animals. This effect was attributed to the elevated preischemic glucose levels. During the early recovery period, the restoration of high-energy phosphates was accelerated by both calcium entry blockers. Nimodipine and emopamil increased the levels of glucose and glucose-6-phosphate in the early postischemic period. Naftidrofuryl (10 mg/kg) increased the level of creatine-phosphate and ATP after 2 min of recovery. Naftidrofuryl (20 mg/kg) exerted no effect on cerebral energy metabolism, but considerably reduced postischemic blood pressure (possibly thereby masking its ameliorative action). Ketamine accelerated the postischemic restoration of high-energy phosphates. In the conscious rat, local cerebral blood flow (LCBF) was determined with the 14C-iodoantipyrine technique following emopamil (20 mg/kg s.c.) or naftidrofuryl (10 mg/kg i.v.) application.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of cerebroprotective agents on cerebral blood flow and on postischemic energy metabolism in the rat brain. 361 Dec 6

The effects of emopamil on postischemic energy metabolism and electroencephalographic (EEG) recovery were investigated in the isolated rat brain perfused at either constant pressure or, alternatively, at constant flow rate. Flow rate and perfusion pressure were monitored continuously. The brains were perfused with a fluorocarbon emulsion for 30 min, and after 30 min of ischemia, perfusion was reinstituted for 5, 30, or 60 min. Global cerebral perfusion rate was increased by emopamil throughout the perfusion period and, accordingly, in brains perfused at a constant flow rate, perfusion pressure was reduced by the drug. At constant pressure perfusion, after 5 min after ischemia, cortical levels of creatine-phosphate, adenosine triphosphate (ATR), glucose, glucose-6-phosphate, and fructose-6-phosphate were higher in emopamil-treated brains than in controls, although the levels of adenosine diphosphate (ADP) and adenosine monophosphate (AMP) were reduced. When brains were perfused at constant flow rate, however, emopamil exhibited no effect on brain energy metabolism in the early reperfusion period. Postischemic restoration of high-energy phosphates proved to depend on the flow rate used. After 30 min of postischemic reperfusion, cortical levels of lactate were lower in emopamil-treated brains compared to controls at both constant pressure and constant volume perfusion. Postischemic lactate levels were independent of flow rate and were also reduced when emopamil was only present during reperfusion. The postischemic restoration of cortical EEG activity was improved by the calcium entry blocker.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of calcium entry blocker emopamil on postischemic energy metabolism of the isolated perfused rat brain. 361 Dec 7

Rat kidneys were made ischemic for 5 to 120 seconds. Segments of individual nephrons were dissected from freeze dried sections and analyzed for ATP, phosphocreatine, glycogen, glucose, glucose-6-phosphate, lactate and creatine kinase. ATP fell most rapidly in proximal convoluted and straight tubules (PCT, PST) and distal convoluted tubules (DCT), and most slowly in glomerulus and papilla. Phosphocreatine levels ranged fivefold and was highest in DCT, where it approached that of brain. Creatine kinase ranged 100-fold with lowest level in PCT, where the ischemic fall in phosphocreatine was so slow as to suggest a function other than that of an energy reserve. Glycogen varied tenfold from modest levels in distal segments to very low levels in PST, and was not used rapidly in any segment. Glucose consumption and lactate production were most rapid in distal portions. High-energy phosphate consumption for the first 7.5 seconds of ischemia, calculated from these data, indicates roughly-equal energy metabolism in proximal and distal segments, with lower levels in papilla, and especially in glomerulus. The absolute values suggest that the in vivo metabolic rate of the nephron continued almost unabated for 5 or 10 seconds of ischemia.
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PMID:Change in energy reserves in different segments of the nephron during brief ischemia. 361 2

To clarify the controversy over whether the neonatal heart is more or less susceptible to global ischemia than the adult heart, the time interval between the onset of ischemia and the beginning of contracture (TIC) was compared in neonatal (n = 6, 3 to 5 days old) and adult (n = 6, 4 to 5 months old) pig hearts. A comparison of the myocardial concentrations (mumol/g wet weight) of ATP, glycogen, lactate, and glucose-6-phosphate (G-6-P) was also done. The anesthetized animals underwent a sternotomy, and control right ventricular myocardial biopsy samples were taken. The heart of each was rapidly excised and placed in a 37 degrees C substrate-free Krebs-Henseleit bath. A compliant balloon was placed in the left ventricle to record pressure changes. Time to onset and peak TIC were recorded and additional proximal right ventricular biopsy samples were taken. Data were recorded as mean +/- SEM. Results demonstrated that neonatal hearts had a significantly shorter (p less than .05) TIC (29.5 +/- 1.7 min) than adult hearts (43.0 +/- 2.9 min) and exhibited more rapid lactate accumulation (2.5 +/- 0.5 to 22.1 +/- 3.0, p less than .001) and an increase in G-6-P (0.07 +/- 0.03 to 0.34 +/- 0.07, p less than .01) with a nonsignificant decline in myocardial glycogen (23.3 +/- 12.1 to 17.4 +/- 4.0, p greater than .05). Our findings indicate that neonatal hearts are more sensitive than adult hearts to global ischemia, which has potential implications for myocardial protection in pediatric cardiac surgery.
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PMID:Relative vulnerability of neonatal and adult hearts to ischemic injury. 366 14

In isolated perfused rat hearts ventricular fibrillation (VF), elicited electrically and persisting further spontaneously, led to an extensive release of creatine kinase (CK). Coronary flow volume and oxygen consumption were increased. In contrast, the CK release was only very small in hearts which were stimulated permanently with rhythmic impulses of 10 Hz, whereas the increase in coronary flow and oxygen consumption was significantly greater. When a relative ischemia was induced by perfusion at a low pressure, the CK release from fibrillating hearts was not greater, but less than at a higher perfusion pressure. It appeared unlikely, therefore, that the CK release from fibrillating hearts was simply due to an oxygen deficiency, although a decrease of ATP and glycogen, and an increase of glucose-6-phosphate and lactate in the myocardium were found. When VF was interrupted by lidocaine, the enzyme leakage was reduced only in the experiments with the higher perfusion pressure. A partial restoration of the myocardial metabolites after 1 h was observed. Findings in maximally ischemic hearts further supported the idea that the enzyme release in fibrillating hearts was not merely due to a lack of oxygen. Complete interruption of the coronary perfusion led to the release of only small CK activities during subsequent coronary reperfusion, whereas the metabolic alterations were more distinct than in fibrillating hearts. Mechanisms responsible for the enzyme release during fibrillation, besides a moderate oxygen deficiency, are discussed.
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PMID:Myocardial damage by ventricular fibrillation in isolated perfused rat hearts, and its underlying mechanisms. 374 57

It is shown in experiments on rats that the early postischemic period after 1- and 1.5-hour ischemia of kidneys is characterized by a decrease in the damage of the glycolytic system site which induces glucose-6-phosphate transformation into lactate and by an increase in the inhibition intensity of the initial hexokinase reaction of glycolysis. In the postischemic period after more prolonged (2-, 3-hour) ischemia the damage of the glycolytic system develops also at the site of glucose-6-phosphate transformation into lactate. Administration either of the nucleotide complex (NAD and AMP) or calmodulin inhibitors (aminazine and zinc sulphate) to rats prior to two-hour occlusion of kidneys vessels promotes a decrease in the inhibition of the glycolytic system activity in the postischemic period. At the same time the separate and combined application of zinc sulphate and triftazin (the most intensive calmodulin inhibitor) is not efficient. The positive effect of NAD, AMP and aminazine on the state of the glycolytic kidney system in the postischemic period correlates with the improvement of the blood microcirculation processes in them.
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PMID:[Glycolysis in the rat kidney shortly after ischemia and administration of calmodulin inhibitors, AMP and NAD]. 379 79

Brain energy state and glycolytic metabolites were measured in young (6 month) and aged (28 month) male rats under normoxic (70% nitrous oxide, 30% oxygen) or hypoxic (PaO2 = 25 mm Hg) test conditions. Hypoxic ischemia was induced in one cerebral hemisphere by ligation of one carotid artery. Under normoxic test conditions brain energy metabolite concentrations were similar between young and aged rats. Brain tissue glucose, glycogen, glucose-6-phosphate and critic acid cycle intermediate concentrations were decreased in aged rats during normoxia while fructose-6-phosphate and pyruvate were increased. Decreases in brain energy state and increases in lactate/pyruvate ratios were significant in both young and aged rats during hypoxia and were greater in aged animals in hypoxic-ischemic tissues. These results indicate that brain energy state is normal in aged rats under normoxic conditions but that hypoxic-ischemia produces a greater degree of brain energy failure compared to younger animals.
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PMID:Brain metabolic changes in young vs aged rats during hypoxia. 404 50

The effect of dihydroergocristine on energy metabolism was studied in the isolated perfused rat brain affected by ischemia and in cultivated C-1300 neuroblastoma cells deprived of oxygen and glucose. Creatine phosphate, ATP, ADP, AMP, glucose, glucose-6-phosphate, fructose-6-phosphate, fructose-1,6-diphosphate, pyruvate, and lactate were measured enzymatically. After a perfusion period of 30 min, the cortex of the isolated perfused rat brain exhibited an energy state not different from that in vivo. Dihydroergocristine added to the perfusion medium (5 mumol/L) did not influence these substrate levels under normal perfusion conditions. However, this drug was able to retard the breakdown of high-energy phosphates during ischemia and to accelerate the restoration of the energy state during the postischemic reperfusion period. The perfusion rate was not changed by the drug, and therefore it was assumed that dihydroergocristine could act directly on cell metabolism. This view was supported by the results obtained from experiments using cultivated N-2a neuroblastoma cells. These cells were incubated in a buffered salt solution deprived of glucose and oxygen for 15 min. Under these conditions, dihydroergocristine (2 mumol/L) added to the incubation medium caused changes in the concentrations or the high-energy phosphates similar to those in the isolated brain preparation: It increased the ATP concentration and decreased the ADP concentration significantly.
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PMID:Effect of dihydroergocristine on energy metabolism studied in the isolated perfused rat brain affected by ischemia and in neuroblastoma cells deprived of oxygen and glucose. 643 25

An isolated working rat heart preparation was used to determine the effect of diltiazem, a calcium antagonist, on the myocardial metabolism and functional recovery in the ischemic and reperfused heart, under conditions of 15 degrees C of topical hypothermia. The hearts were divided into two groups according to the solution injected into aortic root at the onset of ischemia. Group I (25 hearts) were given 3 ml of cold Krebs-Henseleit bicarbonate buffer solution (KHB), and Group II (25 hearts) were given the same dose of KHB containing 300 micrograms of diltiazem. After 30 min of reperfusion following 120 min of ischemia, cardiac output (ml/min) was significantly better in Group II (24.1 +/- 3.2) than in Group I (9.5 +/- 2.5). There were no differences between the groups with regard to tissue levels of creatine phosphate, adenosine triphosphate (ATP), total adenine nucleotide (TAN), glucose-6-phosphate and lactate during the ischemia. However, ATP and TAN levels were significantly higher in Group II after 30 min of reperfusion. These data show that, although diltiazem has little effect in preventing the catabolism of high-energy phosphates during hypothermic ischemia, there was an improvement in myocardial metabolism and an enhanced functional recovery during reperfusion in the diltiazem-treated hearts.
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PMID:Effect of diltiazem on functional recovery and myocardial metabolism during hypothermic global ischemia and normothermic reperfusion. 663 97

Glycolytic substrates and metabolites (glycogen, glucose, glucose-6-phosphate, pyruvate, lactate), tricarboxylic acid cycle intermediates (citrate, alpha-ketoglutarate, succinate, fumarate, malate), related amino acids (glutamate, glutamine, alanine, gamma-aminobutyrate) and energy mediators (ATP, ADP, AMP, creatine phosphate) were evaluated in the cerebral cortex of rats after 5 min of complete compression ischemia as well as after 3, 15 or 30 min of recirculation following 5 min ischemia. The post-ischemic recovery was studied in control animals or in animals treated (30 min before ischemia and during discovery) by intravenous perfusion of vincamine, theophylline, dihydroergocristine and alanine. Interrelated changes of intermediates of the carbohydrate and the amino acid metabolism have been observed. It is concluded that alanine perfusion induced a partial detour of the lactacid anaerobic process towards the succinate-related alactacid cycle, leading to an increase in the cortical gamma-aminobutyrate content. Vincamine and dihydroergocristine acted in the opposite direction.
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PMID:Drug interference on some biochemical parameters of rat cerebral cortex during post-ischemic recovery. 677 99


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