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

After a 30 minute period of superior mesenteric artery occlusion in adult rats, there was a significant decrease in peritoneal inflammatory reaction, ileus, peritoneal adhesion formation, and histologically proved bowel wall necrosis in animals given intravenous dimethyl sulfoxide at the end of the ischemic period. In contrast, control rats given normal saline solution intravenously demonstrated severe inflammatory reaction, ileus, hemorrhagic peritoneal fluid, extensive adhesion formation, and areas of bowel wall necrosis. Intravenous glycerol did not have the beneficial effect seen with dimethyl sulfoxide. Neither compound was effective when given intraperitoneally. We conclude that intravenous dimethyl sulfoxide has a significant protective effect in rats with acute intestinal ischemia due to the superior mesenteric artery occlusion in the rat.
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PMID:Effect of dimethyl sulfoxide and glycerol on acute bowel ischemia in the rat. 396 46

Phosphatic metabolite (perchloric acid extractable) concentrations of cerebral tissues were analyzed by phosphorus-31 nuclear magnetic resonance (P-31 NMR) spectroscopy following external perfusion of the isolated rat brain (30 min or 60 min) under the following conditions: (a) constant perfusion pressure with either fluorocarbon- or erythrocyte-based medium, and (b) constant perfusate flow rate (3 ml/min) with the erythrocyte-based medium. Metabolite concentrations of control perfused brains were compared with those in nonperfused controls to provide a basis for detecting any qualitative or quantitative changes in cerebral metabolite composition. Metabolic responses of perfused brains to ischemia (incomplete ischemia, 83% reduction in flow for 10 min; transient complete ischemia for 1.5 or 2 min) were evaluated immediately after the ischemic episode and at selected time points during reperfusion (3 and 15 min). Alterations in cerebral metabolite levels induced by hypoxia were analyzed using a nonperfused rat brain model. Irrespective of the perfusion method employed, the phosphatic metabolites of control perfused rat brains were identical quantitatively to those of the nonperfused controls. Cerebral ischemia resulted in significantly increased levels of ADP, AMP + IMP, Pi, fructose 1,6-diphosphate, and glycerol 3-phosphate (global ischemia only), whereas ATP and phosphocreatine (PCr) levels declined significantly. The magnitude of these changes varied with the severity of the ischemia; however, following 15 min of control reperfusion metabolite levels had reverted to preischemic values. Significant perturbations in tissue phosphoethanolamine (3.84 delta resonance) content were evident at various time points during ischemia and postischemic recovery, which varied according to the perfusion conditions. In contrast to the changes observed in response to ischemia, hypoxia affected only cerebral high-energy phosphate levels. ATP and PCr levels were reduced, while a concomitant, essentially equimolar, increase in Pi and ADP was observed. The present studies indicate that in terms of phosphatic metabolites, the control equilibrated isolated perfused rat brain is quantitatively and qualitatively indistinguishable from the nonperfused rat brain in vivo regardless of the perfusion conditions (constant flow versus constant pressure). The metabolic responses to ischemia and hypoxia, as measured by P-31 NMR, were consistent with the pattern of changes reported elsewhere. Overall, P-31 NMR spectroscopic evaluation of the intact rat brain provides a potential experimental context for dynamic measures of cerebral metabolism under exogenously controlled conditions. Th
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PMID:P-31 nuclear magnetic resonance analysis of brain: II. Effects of oxygen deprivation on isolated perfused and nonperfused rat brain. 609 45

We have previously reported that the combined administration of mannitol and perfluorochemical blood substitutes is evidently effective in protecting the brain from cerebral ischemia. This experimental study was designed to develop more effective method in suppressing brain infarction than the combined treatment of mannitol and PFC. Using the "Canine model of complete ischemic brain regulated with a perfusion method" in which it is possible to control the degree of blood flow to a cerebral hemisphere via a perfusion pump, the effect of eight agents including six kinds as the free radical scavenger on cerebral ischemia was investigated. Eight agents were mannitol, vitamin E (Vit. E), dimethyl sulfoxide (DMSO), vitamin C, glycerol, nizofenone (Y-9179), dexamethasone (Dexa.) and suloctidil (MY-103). After pretreatment with each agent, blood flow was reduced via the pump to 1/10 of the normal state and 1 hour later, return to the normal state was allowed. Subsequent changes in EEG were observed and the effects of the drugs evaluated. In the control group, no recovery of electrical activity was seen, but in six groups among eight treated groups, i.e., treated with mannitol, Vit. E, DMSO, MY-103, Y-9179 and Dexa, gradual emergence of slow waves was observed. And more favorable effects were found when the combined administration of mannitol, Vit. E and Dexa was made in the same experimental schedule as compared with the single administration of each of these drugs. Furthermore in the animals administered with PFC in combination with mannitol, Vit. E and Dexa, flattening of electrical activity could not be seen throughout the period of severe ischemia. Moreover, the power of electrical activity recovered nearly to the preischemic state immediately after recirculation. Although the possible mechanisms are not yet completely clarified, the present results are thought to indicate that this new combination therapy utilizing PFC with mannitol, Vit. E and Dexa may be useful in the treatment of cerebral ischemia.
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PMID:[Experimental study of cerebral protective effect on cerebral ischemia of various antioxidants and other agents. With special reference to the combined treatment of mannitol, vitamin E, dexamethasone and perfluorochemicals]. 632 77

Male weanling rats were made copper deficient with a purified diet containing all known essential dietary nutrients except copper. Copper deficiency was verified by indirect (anemia, growth retardation, hypercholesterolemia, gross pathology, and abnormal electrocardiograms) and direct (tissue copper analysis) criteria. His bundle electrographic and electrocardiographic changes detected in the copper-deficient group consisted most notably of depressed His-Purkinje system conductivity and S-T segment depression. Phosphorus-31 nuclear magnetic resonance spectroscopic analysis of cardiac, renal, and hepatic tissue perchloric acid extracts revealed significant metabolic changes associated with the dietary copper deficiency, including a generalized marked decrease in ATP and phosphocreatine levels and a corresponding increase in inorganic orthophosphate and ADP levels in the various tissues. Tissue-specific changes consisting of elevated ribose 5-phosphate (heart), phosphocholine (heart), and inosine monophosphate (kidney) and decreased glycerol 3-phosphorylethanolamine (liver) and glycerol 3-phosphorylcholine (liver) levels were detected in copper-deficient rats. Microscopic examination of heart tissue from copper-deficient rats revealed extensive disruption of mitochondrial fine structure, including fragmentation of cristae and inner and outer mitochondrial membranes, which resulted in pronounced vacuolization throughout the tissue. Although the physiological and metabolic disturbances manifested in hearts from copper-deficient animals generally mimic myocardial responses to chronic ischemia, the observed changes are interpreted in a broader context to represent the appearance of a copper-dependent cardiomyopathy.
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PMID:Physiological and metabolic characterization of a cardiomyopathy induced by chronic copper deficiency. 663 5

Brain ischemia was produced in gerbils (Meriones unguiculatus) by the bilateral ligation of the carotid arteries. Definite changes in the energy status of brain demonstrated that carotid occlusion was effective. Five minutes before ligation, an intraventricular injection of either saline or cytidine disphosphate choline (CDP-choline, 0.6 micromol/brain, 3 microliter) was given to groups of animals. Control animals, with and without CDP-choline, together with the ischemic groups, were decapitated directly into liquid nitrogen; 10 min after arterial ligation. Brain free fatty acids, neutral lipids and phospholipids, which were labeled in vivo by the intraventricular injection of [1-14C]arachidonic acid (0.4-0.6 micro Ci, 6-9 nmol) 2 hr prior to ligation, were extracted, purified, and separated by thin-layer chromatographic procedures. The CDP-choline treatment noticeably corrected the increase of total and individual fatty acids due to ischemia and the increase of their radioactivity content. The changes in neutral lipids, particularly in the diacyl glycerol fraction, were also corrected by the injection of the nucleotide. CDP-choline partially reversed the decreased of brain phosphatidylcholine and of its labeling, which was due to ischemia. All the data indicate that the prior injection of CDP-choline stimulates the choline phosphotransferase reaction of brain towards synthesis of phosphatidylcholine and prevents the release of free fatty acids, particularly of arachidonic acid, associated with ischemia.
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PMID:Effect of cytidine diphosphate choline (CDP-choline) on ischemia-induced alterations of brain lipid in the gerbil. 679 97

[2-3H]Glycerol and [1-14C]arachidonic acid were injected into the region of the frontal horn of the left ventricle of mice and were distributed rapidly throughout the brain. After 10 sec, most of the radioactive fatty acid was found in the hemisphere near the injection site; after 10 min, it was recovered in similar proportions in the cerebellum and brain stem. [2-3H]Glycerol showed a heterogeneous distribution, with most of the label remaining in the left hemisphere even after 10 min. On a fresh weight basis, cerebrum, cerebellum, and brain stem were found to contain similar amounts of labeled glycerol. However, the amount of [1-14C]arachidonate in cerebrum was only 50% of that recovered from cerebellum or brain stem. Brain ischemia or a single electroconvulsive shock reduced the spread of the label, producing an accumulation of radioactivity in the injected hemisphere, except for an increase in [2-3H]glycerol in the brain stem during ischemia. Despite the significant decrease in available precursor in the cerebellum and brain stem after electroshock, the amount of label incorporated into lipids was not altered in these areas and only slightly diminished in the cerebrum.
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PMID:Diffusion of intracerebrally injected [1-14C]arachidonic acid and [2-3H]glycerol in the mouse brain. Effects of ischemia and electroconvulsive shock. 682 Apr 76

FFA are the main substrate of biological oxidation in cardiac muscle under normal conditions. But it could be shown in man and animal that during heavy exercise there is a shift to preferential oxidation of lactate. During oxygen deficiency in hypoxic or ischemic situations which may occur lightly in distinct areas of hypertrophic hearts after exercise, lactate, alpha-glycerol phosphate and acyl-CoA as well as triglyceride levels in cardiac tissue may increase, whereas FFA are less oxidized. Unoxidized intracellular FFA and acyl-CoA, which are not esterified in a sufficient way to triglycerides, may impair oxidative phosphorylation in mitochondria, the P/O quotient as well as cardiac function perhaps by an interference with Ca++ movements during the contraction cycle. With the examples of anoxia and complete ischemia as the two extreme situations of O2 deficiency some principles of the alteration of cardiac metabolism are pointed out, and furthermore attempts to improve anoxic tolerance of cardiac tissue.
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PMID:Some aspects on the regulation of carbohydrate and lipid metabolism in cardiac tissue. 699 68

Glycerin-3-P, commonly known as alpha-glycerophosphate and dihydroxyacetone phosphate (DHAP) were measured in well defined microscopic samples of the simple liver acinus allowing a comparison of the glycerin-3-P/dihydroxyacetone-P-ratios of Zones 1 and 3 as a measure of the free NAD+/NADH ratio. The ATP/ADP X Pi quotients were determined in these same microscopic areas of the liver acinus as a measure of the phosphate potential. Brief ischemia was used to disturb the system. The results indicate that the oxidation-reduction and phosphate potentials are uniform throughout the entire liver lobule.
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PMID:Quantitative histochemical resolution of the oxidation-reduction and phosphate potentials within the simple hepatic acinus. 706 1

Hepatic metabolism in intact livers has been studied by 31P nuclear magnetic resonance (NMR) spectroscopy. 31P NMR spectroscopy of normal liver detects little ADP and much lower amounts of inorganic phosphate than are found by enzymatic or chemical analysis. Ischaemia of 30 min duration provokes a rapid fall in ATP to undetectable levels; reflow restores the ATP concentration to 70% of its former level. Intracellular pH changes are qualitatively similar. Fructose and glycerol both cause rapid falls in ATP and inorganic phosphate; these original concentrations are almost restored after 30 min in the case of fructose but not with glycerol where they remain depressed.
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PMID:Hepatic metabolism by 31P NMR. 713 82

Previous studies from our laboratory utilized an isolated isovolumic Langendorff heart preparation to study myocardial metabolism and preservation of left ventricular function following global ischemia and reperfusion. The present study employed a similar preparation to assess the utilization of various glycolytic substrates by monitoring the level of left ventricular developed pressure. Twenty-one rabbit hearts were perfused with an oxygenated but substrate-free Krebs-Ringer-bicarbonate solution in order to deplete the hearts of endogeneous substrate stores. Following a brief period of anoxic, substrate-free perfusion, hearts were perfused with one of seven test substrates under anaerobic, then aerobic conditions. Under anaerobic conditions only perfusion of glucose resulted in a measurable increase in ventricular function which was still less than 20% of control. Under aerobic conditions, provision of glucose, pyruvate, or the combination of alpha-glycerol phosphate and pyruvate resulted in significant increases in contractile function which were 40-70% of control. These results obtained in normal hearts will provide a base line for future studies of the metabolism of postischemic hearts which may have altered cell membrane permeability and/or enzymatic activity.
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PMID:Use of an isolated heart model to test the utilization of substrates for inclusion in cardioplegic solutions. 717 Apr 41


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