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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The study was performed to elucidate whether the biological plasticity of the brain is reduced with advancing age. Both glucose and energy metabolism in the brain cortex of male Wistar rats aged 6, 12, 24 and 30 months were investigated under normal conditions and in 12 and 24 months old rats under complete cerebral ischemia. Under physiological conditions, glucose, fructose-1,6-phosphate and ATP decreased from 6 to 12 months of age whereas pyruvate, malate and creatine phosphate fell from 12 to 30 months of age. It was concluded that glucose and energy metabolism in brain cortex may be slightly reduced with normal aging. Complete cerebral ischemia caused server reduction in cortical glucose, pyruvate, citrate, alpha-ketoglutarate, malate, oxaloacetate, ATP and creatine phosphate and an increase in fructose-1,6-phosphate, lactate, succinate and AMP. Differences between 12 and 24 month old animals became obvious. It is concluded that aged animals as compared to adult animals are not capable of reacting sufficiently to stress conditions. The biological capacity of the brain is assumed to be reduced with aging.
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PMID:[Biologic plasticity of the aging brain]. 376 73

We have already reported that the long-term antihypertensive treatment reduced the degree of cerebral ischemia induced by bilateral common carotid artery ligation (BLCL) in stoke-resistant spontaneously hypertensive rats (SHRSR). This antihypertensive treatment was achieved by the combination of captopril and hydroflumethiazide. In this study, nicardipine hydrochloride which is one of the Ca2+ antagonist was similarly administrated to SHRSR for 8-10 weeks (T-SHR). The effect of long-term antihypertensive treatment by this agent on cerebral ischemia induce by BLCL was investigated and compared with untreated SHRSR (U-SHR). The degree of cerebral ischemia 4 hr after BLCL was estimated by the levels of brain energy metabolites (ATP, lactate, c-AMP) and brain water content. The brain metabolites and water content were measured in the forebrain and hindbrain of each hemisphere. And also the histopathological study on brain vessels 3 hr after BLCL was achieved by using scanning electron microscopy (SEM). The blood pressure of T-SHR gradually declined from 185 +/- 10 mmHg (mean +/- S.D.) to 154 +/- 8 mmHg after 8-10 weeks of antihypertensive treatment. However the blood pressure of U-SHR spontaneously changed from 185 +/- 8 mmHg to 206 +/- 12 mmHg after 8-10 weeks. The blood pressure of T-SHR after the treatment was significantly lower than that of U-SHR. The levels of ATP and c-AMP in T-SHR after BLCL were statistically higher than those in U-SHR, and the lactate levels in T-SHR were significantly lower than in U-SHR in the both fore- and hindbrain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Influence of long-term antihypertensive treatment on cerebral ischemia induced by bilateral common carotid artery ligation in SHRSR--protective effect of nicardipine hydrochloride]. 382 54

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

Three different pressure groups of rats, stroke-prone spontaneously hypertensive rats (SHRSP, 200-270 mmHg), stroke-resistant SHR (SHRSR, 160-240 mmHg), and Wistar rats (WR, 120-160 mmHg) were used to investigate the effect of prior existing hypertension on the severity of brain damage induced by ischemia. The cerebral ischemia was induced by bilateral common carotid artery ligation (BLCL) and the survival rate, cerebral blood flow, cerebral energy metabolites (ATP, lactate c-AMP) and water content were measured. Colloidal carbon perfusion was also performed. Sixteen-week-old male rats were used. The survival rate was observed until 24 hours after BLCL. Cerebral blood flow was measured in parietal cortex by hydrogen clearance method. ATP was measured by luciferin-luciferase method, and lactate by enzymatic method using LDH. c-AMP was measured by radioimmunoassay. Brain water content was measured by freeze-dry method. These measurements were done for animals surviving 6 hours of BLCL. Colloidal carbon perfusion was done according to Ames' Method. The survival rate was lower in the hypertension group. The survival of SHRSP and SHRSR were 20% compared to 71% in WR after 24 hours of BLCL. The cerebral circulation of SHRSP fell abruptly and was near to zero after one hour of BLCL. In SHRSR this fall of cerebral blood flow was prominent in the rats of higher blood pressure. On the other hand there was no apparent fall of cerebral blood flow in WR after BLCL. The cerebral energy metabolites. ATP and c-AMP showed the lowest level in SHRSP which had the negative correlation to blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Experimental cerebral ischemia after bilateral common carotid artery ligation in SHRSP, SHRSR and Wistar rats: correlation between blood pressure and degree of ischemia]. 609 92

The effects of global cerebral ischemia on neurochemical parameters in the brain were examined in rats. Global cerebral ischemia was produced by temporary occlusion of the bilateral common carotid arteries 24 hr after the permanent electrocauterization of the bilateral vertebral arteries. In 10-min cerebral ischemic rats, the brain levels of monoamine were unaltered. The brain levels of gamma-aminobutyric acid (GABA), which increased about 1.5-fold just before recirculation, almost recovered to the levels of the sham operated group (sham ope. levels) within 5 min after recirculation. The brain levels of cyclic AMP (cAMP), although they altered a little just before recirculation, increased about 6-fold 1 min after recirculation, and they recovered to the sham ope. levels 3-5 min later. In 30-min cerebral ischemic rats, the brain levels of monoamine decreased to about 40% of the sham ope. levels just before recirculation, and norepinephrine (NE) and 5-hydroxytryptamine (5-HT) levels did not recover within 30 min after recirculation in the telencephalon. The brain GABA levels which increased about 2-fold just before recirculation, recovered to the sham ope. levels in all brain regions by 30-min recirculation except for the levels in cerebral cortex and cerebellum. The brain cAMP levels which increased about 3.5-fold 10 min after recirculation, almost recovered 20 min later. However, the cAMP levels in the telencephalon decreased to levels lower than the sham ope. levels 30 min after recirculation. It is suggested that the changes of these neurochemical parameters in the telencephalon are related in part to the abnormalities of behavior and EEG activity which have been already reported.
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PMID:[Neurochemical study of the temporary cerebral ischemic rats produced by bilateral vertebral and carotid artery occlusion]. 615 38

Norepinephrine (NE) depletion of the cerebral cortex after lesion of the ipsilateral locus ceruleus (LC) causes abnormalities of cerebral oxidative metabolism when the cortex is stimulated to increased energy demand (Harik, S. I., J. C. LaManna, A. I. Light, and M. Rosenthal (1979) Science 206: 69-71; LaManna, J. C., S. I. Harik, A. I. Light, and M. Rosenthal (1981) Brain Res. 204: 87-101). These abnormalities were exhibited as decreased mitochondrial reducing equivalent flow. One possible cause of this would be the decreased availability of oxidative metabolic substrates in the NE-depleted cortex. We therefore investigated the effect of unilateral LC lesion and the resultant depletion of ipsilateral endogenous NE on glycogen and other energy metabolites in the cerebral cortex of rats under three conditions: (1) at "rest," (2) when energy demand is inncreased markedly by seizures, and (3) during total cerebral ischemia. We report no differences in cerebral metabolites between NE-depleted and control hemispheres at "rest." In seizures and ischemia, however, the increase in the level of adenosine 3':5'-monophosphate (cyclic AMP) and the breakdown of glycogen were impaired considerably in the NE-depleted cortex. The data suggest that depletion of central NE impairs cerebral glycogenolysis in response to increased energy demands and ischemia. Such impairment may be mediated via a cyclic AMP-related mechanism.
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PMID:Norepinephrine regulation of cerebral glycogen utilization during seizures and ischemia. 627 95

We tested whether cerebral noradrenaline (NA) may play a central role in mediating the increased production of free fatty acids (FFAs) during cerebral ischemia. Levels of FFAs, cyclic AMP, and NA, as well as ATP, ADP, and AMP, were measured in cerebral cortex during decapitation ischemia in rats 2 weeks after unilateral locus ceruleus lesion. Comparisons were made between the results obtained from the contralateral cortex with normal NA content and the NA-depleted ipsilateral cortex. Although NA depletion was associated with a diminished transient rise of cyclic AMP in response to ischemia, it failed to influence the magnitude of FFA increase or the decline of energy state within the 15-min period of ischemia. A more than twofold increase of total FFAs (sum of palmitic, stearic, oleic, arachidonic, and docosahexaenoic acids) was observed in both hemispheres at 1 min after decapitation, when energy failure became manifest. The increased production of FFAs continued throughout the 15 min of ischemia, with a preferential rise in the levels of stearic and arachidonic acids. There was an inverse correlation between FFA levels and total adenylate pool. The results do not support a major role for NA and cyclic AMP in increasing cortical FFAs during complete ischemia. Instead, they are consistent with the view that impaired oxidative phosphorylation activates deacylating enzymes. Disturbance of reacylation due to energy depletion is probably another factor contributing to the continuous increase of FFAs during prolonged ischemia.
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PMID:Free fatty acids and energy metabolites in ischemic cerebral cortex with noradrenaline depletion. 631 5

The objective of this study was to assess the relationship between the changes in the redox state of cytochrome oxidase (Cyt. ox.) and those of spontaneous EEG activity and cellular energy state during cerebral ischemia and recirculation. We induced 5-min forebrain ischemia by occluding the bilateral common carotid arteries in anesthetized gerbils. Redox changes of Cyt. ox. were monitored with near-infrared spectroscopy (NIRS) through the experiments. Cortical energy metabolites, ATP, ADP, and AMP, were also measured with high performance liquid chromatography (HPLC) during ischemia and recirculation. Ischemia immediately caused a rapid reduction of Cyt. ox., which paralleled to deterioration of spontaneous EEG activity and preceded significant changes in cellular energy state. Re-oxygenation of Cyt. ox. was observed just after recirculation, and paralleled to the recovery of cellular energy state. Spontaneous EEG activity did not recover even when all other NIRS parameters almost recovered during recirculation after 5-min ischemia. During clamping of the carotid artery, NIRS findings also correlated with those of somatosensory evoked potential (SEP). We concluded that, by means of monitoring redox changes of Cyt. ox., NIRS can detect non-invasively critical neuronal hypoxia prior to a significant impariment of cellular energy state caused by cerebral ischemia, and that NIRS can also detect recovery of oxidative phosphorylation during recirculation, which cannot be observed on EEG.
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PMID:[Near-infrared monitoring of cerebral oxygenation during cerebral ischemia]. 759 May 92

We examined the effects of rolipram, a cyclic AMP-selective phosphodiesterase inhibitor, on cerebral ischemia-induced neuronal damage in Mongolian gerbils. Transient forebrain ischemia was induced by 3-min occlusion of bilateral common carotid arteries. Rolipram, at a dose of 0.3 or 3 mg/kg, was injected i.p. 30 min before ischemia. Histopathological observations showed that neuronal damage to the hippocampal CA1 subfield, which was seen 7 days after ischemia in vehicle-treated animals, was reduced in animals treated with the higher dose of rolipram.
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PMID:Rolipram, a cyclic AMP-selective phosphodiesterase inhibitor, reduces neuronal damage following cerebral ischemia in the gerbil. 771 41

The present study investigated the effect of the administration of oxypurinol (40 mg/kg), an inhibitor of xanthine oxidase, on adenosine and adenine nucleotide levels in the rat brain during ischemia and reperfusion. The brains of the animals were microwaved before, at the end of a 20-min period of cerebral ischemia, and after 5, 10, 45, and 90 min of reperfusion. Cerebral ischemia was elicited by four-vessel occlusion with arterial hypotension to 45-50 mm Hg. Adenosine and adenine nucleotide levels in the oxypurinol-pretreated (administered intravenously 20 min before ischemia) rats were compared with those in nontreated animals exposed to the same periods of ischemia and reperfusion. Oxypurinol administration resulted in significantly elevated ATP levels at the end of ischemia and 5 min after ischemia, but not at 10 min after ischemia. ADP levels were also elevated, in comparison with those in the control rats, at the end of the ischemic period. Conversely, AMP levels were significantly reduced at the end of ischemia and during the initial (5 min) period of reperfusion. Adenosine levels were lower in oxypurinol-treated rats, during ischemia, and in the initial reperfusion phase. Oxypurinol administration resulted in a significant increase in the energy charge both during ischemia and after 5 min of reperfusion. Physiological indices, namely, time to recovery of mean arterial blood pressure and time to onset of respiration, were also shortened in the oxypurinol-treated animals. These beneficial effects of oxypurinol may have been a result of its purine-sparing (salvage) effects and of its ability to inhibit free radical formation by the enzyme xanthine oxidase. Preservation of high-energy phosphates during ischemia likely contributes to the cerebroprotective potency of oxypurinol.
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PMID:Oxypurinol-enhanced postischemic recovery of the rat brain involves preservation of adenine nucleotides. 772 3


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