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

Effects of S-adenosyl-L-methionine (SAMe).2 sulphate.tosylate upon the ischemia-induced brain edema and survival rate in Mongolian gerbils and spontaneously hypertensive rats were investigated, since SAMe is known to be important as a physiologically active substance in numerous metabolic processes including those that are inhibited in ischemia. SAMe suppressed increases in water and Na+ content in the ischemic brain which was produced by ligation of the common carotid artery for a short term (20-30 min) in Mongolian gerbils. This ameliorating effect of SAMe was observed dose-dependently at higher doses than 100 mg/kg administered repeatedly every 0.5 or 1 hr, starting within 2 hr, at least, after the reperfusion. Similar effects were also obtained in spontaneously hypertensive rats whose common carotid artery on both sides were ligated permanently. SAMe also increased survival rate in Mongolian gerbils with ischemic brain. Although the SAMe solution employed in the present experiments was hypertonic and contained mannitol as a filler, the beneficial effects were due to neither the hypertonicity of the solution nor mannitol, but due to SAMe itself.
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PMID:Effects of S-adenosyl-L-methionine upon ischemia-induced brain edema in Mongolian gerbils and spontaneously hypertensive rats. 313 70

Oxygen-derived free radicals have been shown to be important mediators in ischemia-reperfusion injury to skin flaps. Agents that reduce the level of these free radicals have been used to improve flap survival in model systems. An in vitro study of the interactions between amino acids and hydroxyl radicals by electron spin resonance spectroscopy suggests an intrinsic radical scavenging activity of certain amino acids. The ability of these amino acids to improve acute axial-random skin flap survival was examined in a rat model. Cysteine, methionine, proline, hydroxyproline, histidine, and phenylalanine, given intravenously, significantly improved flap survival over saline controls; alanine gave an intermediate result, while aspartic acid showed no improvement. The in vitro data were generally a good predictor of free radical scavenging ability as manifested by improved flap survival in vivo. Biochemical mechanisms and clinical applications are described.
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PMID:Improved survival of acute skin flaps with amino acids as free radical scavengers. 319 Aug 67

We investigated the effect of S-adenosyl-L-methionine (SAMe) on the prevention of the delayed neuronal death in rats subjected to transient and brief forebrain ischemia. As the results, SAMe dose-dependently protected the hippocampal CA1 neurons from degeneration and necrosis, whose effect was suppressed by simultaneous administration of S-adenosyl-L-homocysteine, a potent inhibitor in transmethylation. No protective effect was observed in CDP-choline, phosphatidylcholine and L-methionine. Therefore, it is necessary for the prevention of the delayed neuronal death to enhance cerebral SAMe level and to activate transmethylation using SAMe as a methyl donor in postischemic brain.
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PMID:S-adenosyl-L-methionine protects the hippocampal CA1 neurons from the ischemic neuronal death in rat. 333 27

The effect of S-adenosyl-L-methionine sulfate tosylate (FO-1561) on survival time in various brain damage models (cerebral anoxia or ischemia) was studied. 1) In KCN-induced or normobaric anoxia of ddY mice, FO-1561 (30-100 mg/kg as amount of S-adenosyl-L-methionine) administered intravenously 15-30 min prior to the treatment showed significant increase of survival time dose-dependently. 2) In asphyxic anoxia of Wistar rats, FO-1561 (100 mg/kg) administered intravenously 15 min prior to the treatment (cessation of artificial respiration) delayed the time until the disappearance of electrocorticogram. 3) In cerebral ischemia of Mongolian gerbils, FO-1561 (50 mg/kg) injected five times at 1 hr interval intraperitoneally 3 hr after the unilateral ligation of common carotid arteries showed significant increase of survival time. These results suggested that FO-1561 may be effective in ameliorating cerebral anoxic or ischemic damage, without observing any side effects like sedation and motor depression which pentobarbital showed with the effective doses in these damage models.
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PMID:[The effect of S-adenosyl-L-methionine sulfate tosylate (FO-1561) on survival time in various brain damage models]. 340 5

The effect of S-adenosyl-L-methionine (SAM) on neuronal degeneration induced by transient forebrain ischemia was studied in rats. Bilateral occlusion of the common carotid arteries for 30 min in a 4-vessel occlusion model caused degeneration of CA1 neurons of the hippocampus. When SAM-HCl or SAM sulphate tosylate (SAM-ST, 100 mg/kg as the free form of SAM, i.p.) was administered just after recirculation and every hour for 5 h after recirculation, the degeneration and loss of pyramidal cells were prevented. However, adenosine, a metabolite of SAM, and glycerol, which has the same osmotic pressure as the solution of SAM-ST, did not show any effects on the neuronal damage. The results showed that SAM has a beneficial effect on neuronal damage induced by ischemia.
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PMID:S-adenosyl-L-methionine prevents ischemic neuronal death. 343 68

Effects of S-adenosyl-L-methionine (SAM) on the improvement of cerebral energy metabolism and microcirculation were examined in postischemic rat brain. Male Wistar rats, whose vertebral arteries were electrically cauterized last day, were subjected to forebrain ischemia by temporary clipping of both common carotid arteries. After 60 min of ischemic insult, they were intravenously administered with SAM at doses of 30 or 100 mg/kg; this was followed by recirculation for 60 min. To determine cerebral concentrations of energy metabolites, the brain was frozen in situ. Adenine nucleotides (ATP, ADP, AMP) were assayed by anion-exchange HPLC system, and other metabolites (PCr, glucose, lactate, pyruvate) were analyzed by enzymatic fluorometry. In order to estimate regional cerebral blood flow (rCBF) and glucose utilization, double-tracer autoradiography was undertaken using 14C-iodoantipyrine (14C-IAP) and 18F-fluorodeoxyglucose (18F-FDG). In animals without SAM treatment (60-60 group), energy metabolites did not recover and neither CBF nor glucose uptake restored during 60 min of recirculation. In contrast, in SAM-treated animals (60-60 SAM group), values of the energy metabolites improved significantly and both CBF and glucose uptake recovered, though incompletely. These results indicate that SAM is able to improve postischemic cerebral microcirculation and energy metabolism. For mechanisms of the effects, it is suggested to the enhancement of erythrocyte deformability by phospholipid methylation, the stabilization of mitochondria, and the normalization of injured metabolic reactions. Therefore, we conclude that SAM is able to be effective clinically as a drug treated for the acute phase of cerebrovascular diseases.
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PMID:[Effects of S-adenosyl-L-methionine on the cerebral energy metabolism and microcirculation in the rats subjected to transient forebrain ischemia]. 344 52

This study examines protein synthesis in heterotopically transplanted rat hearts and several tissues of recipient rats. Donor hearts and recipient tissues synthesized many of the normally occurring proteins observed in tissues of unstressed rats. In addition, a stress-induced protein with a molecular mass of 71 kilodaltons was synthesized in donor heart, recipient heart and lung. Donor hearts incorporated more L-[35S]-methionine than did recipient hearts. Tissues of recipient rats also incorporated more label than the respective tissues of sham-recipient rats. These results suggest that ischemia, endured by the donor hearts during transplantation, induced these changes in protein synthesis.
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PMID:Protein synthesis in heterotopically transplanted rat hearts. 355 78

Changes in biochemical and electroencephalographic parameters were followed over time during the development of acute hepatic encephalopathy (HE) in two different experimental models. In the rat, (sub)acute liver failure was obtained either by ligation of the hepatic artery in previously portacaval-shunted animals or by intraperitoneal injection of a high dose of galactosamine (GALN). The EEG changes were characterized in both models by a significant increase in low-frequency activity of the EEG power density spectra: the so-called 'left shift'. This 'left shift' was significant in liver ischemia after 4-5 h and in GALN hepatitis after about 30 h. The changes in plasma biochemical indices also showed a great similarity in both models. The concentration of all measured plasma amino acids (except histidine and arginine in GALN hepatitis and arginine in liver ischemia), NH3 and ALAT were significantly increased during the development of (sub)acute HE. Correlation of the combined data of electroencephalographic and biochemical indices showed a significant (P less than 0.01) correlation between the 'left shift' and NH3, taurine, threonine, proline, alanine, methionine, cystathionine, phenylalanine, tryptophan, ornithine and histidine. It is concluded that EEG spectral analysis is a useful parameter for following the development of (sub)acute hepatic encephalopathy in relation to biochemical parameters.
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PMID:Correlation between electroencephalographic and biochemical indices in acute hepatic encephalopathy in rats. 359 63

This study examined the pattern of protein synthesis in the neocortex, caudate-putamen, and the hippocampus following transient forebrain ischemia in rats. The animal model of temporary ischemia used in this study causes permanent damage to vulnerable neurons with a time course of injury that varies from hours (caudate nucleus) to days (hippocampus). To examine the spectrum of proteins synthesized in these regions at 3 and 18 h after recirculation, cerebral proteins were pulse-labeled in vivo by an intravenous injection of [35S]methionine. Newly synthesized (35S-labeled) and constitutive (unlabeled) proteins were analyzed by two-dimensional gel electrophoresis and fluorography. In all three brain regions, specific proteins underwent preferential synthesis (Mr approximately 27,000, approximately 65,000, approximately 70,000, approximately 110,000), while others showed decreased synthesis (neuron-specific enolase, alpha- and beta-tubulin). There was an early (3 h post ischemia) induction of the Mr approximately 70,000 mammalian "stress" protein; at 18 h post ischemia, its synthesis remained high in the hippocampus but was diminished in the neocortex and had largely subsided in the caudate-putamen. All regions at 18 h showed increased synthesis of an Mr approximately 50,000 protein, tentatively identified as glial fibrillary acidic protein. The results show that temporary forebrain ischemia induces changes in protein synthesis that include features similar to those observed in other eukaryotic cells subjected to injurious stress. These postischemic changes in protein synthesis are qualitatively similar in all brain regions examined despite regional differences in the severity of subsequent neuronal damage. The persistent synthesis of the Mr approximately 70,000 stress protein in the hippocampus, however, may reflect continued metabolic injury long after the ischemic episode has passed.
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PMID:Protein synthesis in postischemic rat brain: a two-dimensional electrophoretic analysis. 379 99

Effects of S-adenosyl-L-methionine sulfate tosylate (FO-1561) on postischemic cerebral functional and metabolic recovery in experimental cerebral ischemia were investigated. Severe bilateral forebrain ischemia in rats was induced by four-vessel occlusion with reducing the mean arterial pressure to 100-110 mmHg. After forebrain ischemia had been maintained for 30 minutes, recirculation was started by removal of the arterial clamps of bilateral common carotid arteries and by increasing systemic arterial pressure to the preischemic level. The EEG was continuously recorded from gold-coated screws inserted bilaterally in the parietal bones with the tips in extradural position, against a reference inserted prefrontal bone. Analysis of power spectrum of EEG activity was done by Berg Fourier Analyser. The brains were frozen in situ with liquid nitrogen before, during and after ischemia and then chiselled out during irrigation with liquid nitrogen. Concentrations of ATP in brain tissue were determined with high performance liquid chromatography. FO-1561, 100 mg/kg, was given intravenously, immediately after recirculation. After recirculation there was a tendency that EEG power spectrum in FO-1561-treated animals contained higher percentage of beta wave compared to that in control animals, while delta wave was lesser in FO-1561-treated animals. At 90 minutes following recirculation, ATP level in control animals was 2.17 +/- 0.05 mumol/g (mean +/- SE) and 2.42 +/- 0.03 mumol/g (mean +/- SE) in FO-1561-treated animals. Thus, recovery of ATP level was significantly better in FO-1561-treated animals than in control animals (p less than 0.01).
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PMID:[Effects of FO-1561 on postischemic cerebral functional and metabolic recovery in experimental cerebral ischemia]. 381 37


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