Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Normothermic rats with 12 min, complete cerebral ischemia were treated with the AMPA antagonist 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo (F) quinoxalinedione (NBQX) [10], which prevents CA1 pyramidal neuron loss. Twenty hours after ischemia, cerebral protein synthesis rate (CPSR) was measured autoradiographically using [35S]methionine. Ischemia caused a 38% decrease of CPSR in CA1, and postischemic treatment with NBQX caused a 66% decrease in this region. Also treatment with NBQX alone resulted in a decrease (22% in CA1) of the CPSR. Since some evidence exists that the neuroprotective effect of NBQX is related to blockade of the fast AMPA-mediated transmission, the further decrease of the postischemic CPSR in CA1 could be a mere side effect.
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PMID:Regional cerebral protein synthesis after transient ischemia in the rat: effect of the AMPA antagonist NBQX. 138 88

Effects of S-adenosyl-L-methionine (SAM) on the metabolism in ischemic brain were investigated. The ischemic model employed was an incomplete cerebral ischemia of the spontaneously hypertensive rat (SHR) produced by the occlusion of both common carotid arteries. One hundred mg/kg of SAM was administered (i.p.) 6 times from the beginning of occlusion at 30 min intervals. At 3 hr after the onset of occlusion, animals were killed by microwave irradiation and creatine phosphate (CrP), ATP, glucose, lactate and gamma-aminobutyric acid (GABA) contents in the brain were measured. SAM significantly mitigated both the reductions in CrP, ATP and glucose levels and the increase in GABA level due to the cerebral ischemia. In another set of experiments with the same experimental schedule, water content in the brain was examined. SAM significantly suppressed the increase in water content due to the cerebral ischemia. These results indicate ameliorating effects of SAM on the metabolism in ischemic brain.
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PMID:S-adenosyl-L-methionine ameliorates ischemic brain metabolism in spontaneously hypertensive rats. 273 57

A repeated acquisition procedure in a 3-panel runway apparatus was used to investigate the effects to S-adenosyl-L-methionine (SAM) on impairment of working memory produced either by cerebral ischemia or by scopolamine in rats. Cerebral ischemia (2-10 min) produced duration-dependent increases in the number of errors (pushes made on the two incorrect panels located at each choice point) and increased latency (time before the rat reached the goal box). The increase in errors induced by a 5 or 10 min period of ischemia decreased gradually in subsequent training sessions, returning to the control levels in 6 days. The increases in both errors and latency induced by 5 min of ischemia were significantly reduced by 100 and 180 mg/kg SAM administered i.p. immediately after blood recirculation and 1 h before a test conducted 24 h after ischemia. SAM at doses up to 180 mg/kg nevertheless failed to reduce the increases in errors and latency if they were induced by 0.56 mg/kg of scopolamine. These results suggest that SAM has a beneficial effect on memory that has been impaired by cerebral ischemia.
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PMID:Effect of S-adenosyl-L-methionine on impairment of working memory induced in rats by cerebral ischemia and scopolamine. 279 91

We investigated the participation of endogenous opioid peptide in cerebral ischaemia. In 13 patients with supratentorial infarction, the plasma immunoreactive methionine-enkephalin concentration at the acute stage (30.77 +/- 3.54 pg/ml) was significantly higher than that at the chronic stage (20.37 +/- 2.07 pg/ml) or that of the control subjects (19.64 +/- 1.71 pg/ml). However, it was unrelated to infarct size or patient severity. The increased methionine-enkephalin, which appears to originate from the sympatho-adrenal system or infarcted brain, may play a role in the evolution of cerebral ischaemia.
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PMID:Increase of plasma methionine-enkephalin levels in patients at the acute stage of cerebral infarction. 290 26

We investigated the effects of intravenous application of nimodipine on the neurophysiologic, biochemical, and morphologic consequences of 15 minutes of global cerebral ischemia in seven rabbits. In vivo dialysis of the hippocampus was used to determine changes in extracellular concentrations of extracellular calcium and amino acids and blood-brain barrier permeability. Ischemia without treatment produced a rapid disappearance of electroencephalographic activity, a decrease in the concentration of extracellular calcium, the release of neuroactive amino acids, and leakage of methionine to the tissue fluid, plus a significant increase of the blood-brain barrier permeability to fluorescein. Except for permeability and electroencephalographic activity, these parameters normalized during 45 minutes of recirculation; permeability and activity failed to normalize completely during 3 hours of recirculation. After 3 hours of recirculation, morphologic changes in the CA1 hippocampal area were observed. Treatment with nimodipine significantly enhanced electroencephalographic activity recovery and normalization during recirculation, reduced the decrease in extracellular calcium concentration, and prevented the increased permeability of the blood-brain barrier. Nimodipine protected the CA1 area from early morphologic changes and reduced leakage of methionine from brain cells. The beneficial cytoprotective effect of nimodipine, probably related to normalization of calcium homeostasis and blood-brain barrier permeability after ischemia, may reflect both vascular and cellular sites of action.
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PMID:Beneficial effect of nimodipine on metabolic and functional disturbances in rabbit hippocampus following complete cerebral ischemia. 291 38

Effects of S-adenosyl-L-methionine (SAMe) on experimental cerebral ischemia were investigated using two different ischemic models. Cerebral energy metabolites (ATP, lactate, c-AMP) and brain water content were measured. It is reported that SAMe accelerates synthesis of phosphatidyl choline and increases erythrocyte membrane fluidity. Complete ischemia was produced by heart excision using wistar kyoto rats. SAMe (100 mg/kg, I.P.) was administered twice at one hour and immediately before inducing ischemia. The brain of rats were irradiated by microwave to stop the enzyme activity exactly 60 seconds after inducing ischemia and brain energy metabolites were measured. Recirculation model was produced by one hour recirculation following two hours ischemia induced by clipping of bilateral common carotid arteries using stroke-prone spontaneously hypertensive rats. SAMe (100 mg/kg, I.V.) was administered twice one hour after clipping and ten minutes after recirculation. The brain metabolites and water content were measured one hour after recirculation. In the complete ischemia, ATP and c-AMP levels were statistically high in the SAMe treated group compared to the untreated group (vehicle). But there was no statistical difference in lactate between the treated group and the untreated group. In the recirculation model, lactate elevation was suppressed in the SAMe treated group compared to the vehicle group with statistical difference, but there was no difference in ATP and c-AMP. Also, there was no difference in water content between the treated and the untreated group. SAMe protected energy failure in ischemia and accelerated recovery from ischemia. It is indicated that this agent is beneficial for treatment of cerebral ischemia in the acute stage.
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PMID:[Effects of S-adenosyl-L-methionine on experimental cerebral ischemia]. 299 May 9

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

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

Neuronal protein synthesis is severely depressed following stress such as heat-shock, hypoxia, and hypoglycemia. Following reversible cerebral ischemia, protein synthesis is transiently inhibited in ischemia-resistant areas, but persistently depressed in vulnerable brain regions. Eukaryotic initiation factor 2 (eIF-2) activity, that is, the formation of the ternary complex eIF-2.GTP.initiator 35S-Met-tRNA, a rate-limiting step in the initiation of cellular protein synthesis, was studied in the rat brain during and following 15 min of transient global cerebral ischemia. At 30 min and 1 hr of reperfusion, a general decrease of eIF-2 activity by approximately 50% was seen in the postmitochondrial supernatant (PMS). In the relatively resistant neocortex and CA3 region of the hippocampus, the eIF-2 activity returns to control levels at 6 hr of reperfusion, but remains depressed in the vulnerable striatum and the CA1 region. Similarly, the activity of the guanine nucleotide exchange factor (GEF), which catalyzes the exchange of GTP for GDP bound to eIF-2, a crucial step for the continued formation of the ternary complex, is transiently reduced in neocortex but persistently depressed in striatum. The postischemic decrease in eIF-2 activity is further attenuated by agarose-bound alkaline phosphatase, and mixing experiments revealed that a vanadate-sensitive phosphatase may be responsible for the depression. Addition of partially purified GEF to PMS from postischemic neocortex restored eIF-2 activity to control levels. We conclude that ischemia alters the balance between phosphorylation and dephosphorylation reactions, leading to an inhibition of GEF and a depression of ternary complex formation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Stress-induced inhibition of protein synthesis initiation: modulation of initiation factor 2 and guanine nucleotide exchange factor activities following transient cerebral ischemia in the rat. 847 77

We have studied the beneficial effects of S-adenosyl-L-methionine (SAM) tosylate on blood-brain barrier (BBB) breakdown and neuronal survival after transient cerebral ischemia in gerbils. BBB breakdown experiments were performed in pentobarbital anesthetized gerbils subjected to 10 min of bilateral carotid artery occlusion and 6 h of reperfusion. For BBB breakdown measurements, SAM (120 mg/kg, i.p.) was administered to gerbils just after occlusion and thereafter every hour up to 5 h. Fluorometric measurements quantified the blood-brain permeability tracer, Evans blue (EB). SAM treatment significantly reduced the BBB breakdown as indicated by reduced levels of EB fluorescence. Neuronal count experiments were conducted in gerbils subjected to transient ischemia and 7 days of reperfusion. For neuronal count experiments SAM (15-120 mg/kg) was administered at 6 and 12 h after reperfusion, and twice each day thereafter for 7 days. SAM dose dependently protected the hippocampal CA1 neurons assessed by histopathological methods. SAM has a beneficial effect on the outcome of ischemic injury by reducing the BBB breakdown and neuronal death.
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PMID:Beneficial effects of S-adenosyl-L-methionine on blood-brain barrier breakdown and neuronal survival after transient cerebral ischemia in gerbils. 903 Jul 7


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