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

Potential involvement of neuroexcitatory mechanisms was studied in: 1) repetitive forebrain ischaemia in gerbils, 2) global cerebral ischaemia in rats and 3) cryogenic injury to the cerebral cortex in rats and gerbils. Uptake of 45Ca was used as a marker of injury, whereas ultrastructural localization of calcium was assessed with an oxalate-pyroantimonate method. The blood-brain barrier was evaluated with immunostaining for serum albumin. Changes in extracellular glutamate were estimated by microdialysis and an enzymatic cycling assay. Changes in water content were assessed by specific gravity measurements. Repetitive ischaemia of 3 x 5 min carotid occlusions produced a cumulative effect with regard to development of oedema and neuronal injury. This was associated with several-fold increments in glutamate release after repeated insults, whereas there was no apparent correlation with energy metabolism disturbances. Other studies revealed in all models a development of secondary foci distant to the primary impact of ischaemia or cold lesions, which were characterized by calcium accumulation in swollen dendrites, chronic neuronal changes and intraneuronal uptake of serum proteins, all of these changes being potentially compatible with involvement of neuroexcitatory mechanisms.
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PMID:Role of neuroexcitation in development of blood-brain barrier and oedematous changes following cerebral ischaemia and traumatic brain injury. 198 78

The present study was designed to elucidate possible therapeutic effects of naftidrofuryl on the brain glucose metabolism after cerebral ischemia. Cerebral ischemia was induced by injecting 680 microspheres with a diameter of 48 microns into the right internal carotid artery of the rat. After ensuring the onset of symptoms of stroke on the first day after the operation, the rats were treated with intraperitoneal injections of 15 mg/kg naftidrofuryl oxalate twice a day. The behavioral and metabolic changes of operated rats were monitored up to the 5th day after surgery. The symptoms gradually faded away, from the 3rd day on, after microsphere-induced cerebral embolism. Tissue glucose and glycogen greatly increased after cerebral embolism, suggesting embolism-induced inhibition of glycolysis. To elucidate which steps in the glycolytic catabolism are inhibited after cerebral ischemia, biochemical activities of the glycolytic enzymes in the Embden-Meyerhof pathway and tricarboxylic acid cycle were determined on the 3rd day after surgery. Enzyme activities of hexokinase, phosphofructokinase and pyruvate kinase were not inhibited, but rather increased slightly after cerebral embolism. Malate dehydrogenase activity in the brain mitochondria was markedly increased after microsphere-embolism, whereas other enzyme activities in the tricarboxylic acid cycle were never inhibited by the cerebral embolism. Treatment of naftidrofuryl resulted in an appreciable reverse of the brain glucose and glycogen levels and a substantial recovery of altered enzyme activities to normal levels in the Embden-Meyerhof pathway and tricarboxylic acid cycle.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Naftidrofuryl oxalate improves impaired brain glucose metabolism after microsphere-induced cerebral embolism in rats. 201 99

Using the oxalate-pyroantimonate technique ultrastructural localization of Ca2+ was determined in the nucleus supraopticus, the nucleus paraventricularis and in the neurohypophysis after complete cerebral ischemia. We observed an increased calcium accumulation in mitochondria of some neurons. Calcium precipitate was also found in vesicles, in cytoplasm of neurons and their swollen dendritic processes. Abundant Ca2+ precipitate occurred in synaptic vesicles and within synaptic cleft. It was present between disjuncted lamellae of the myelin sheath in profiles of myelinated axons present in neuropil. Diffuse precipitate was visible in the cytoplasm of pituicytes, as well as in microvesicles in the neurohypophysis. The possible role of calcium in ischemia is briefly discussed.
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PMID:Cytochemical calcium localization in hypothalamo-neurohypophysial system of rats after ischemia. Preliminary observations. 262 94

1. The present study was designed to determine whether naftidrofuryl oxalate exerts a possible therapeutic effect on brain energy metabolism impaired by microsphere-induced cerebral embolism in vitro. 2. Injection of microspheres into the right carotid canal resulted in a decrease in tissue high-energy phosphates both in the right and left hemispheres, and an increase in tissue lactate in the right hemisphere, on the 3rd and the 5th day after the embolism. The embolism also induced a marked reduction in mitochondrial oxidative phosphorylation ability and succinate dehydrogenase activity. The results suggest that severe ischaemia was induced in the brain by the microsphere administration. 3. Treatment of microsphere-injected rats with naftidrofuryl oxalate (15 mg kg-1) for 3 or 5 days elicited a significant recovery of tissue high-energy phosphate and lactate levels. The recovery was associated with a significant restoration of mitochondrial succinate dehydrogenase activity on the both days and of mitochondrial oxidative phosphorylation rate on the 5th day. 4. The results suggest that naftidrofuryl oxalate is beneficial in the recovery of cerebral energy metabolism impaired by microsphere-induced cerebral ischaemia, presumably through a mechanism involving its direct effect on the cerebral mitochondrial enzyme activities.
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PMID:Possible therapeutic effect of naftidrofuryl oxalate on brain energy metabolism after microsphere-induced cerebral embolism. 281 26

1. The purpose of the present study was to determine whether naftidrofuryl oxalate (naftidrofuryl), a vasodilator, is capable of improving brain regional blood flow of animals in sustained ischaemia. 2. Cerebral ischaemia was induced by injecting 900 microspheres (48 microns in diameter) into the right internal carotid artery of rats. Cerebral blood flow of brain regions was measured by a hydrogen clearance method on the 3rd, 7th and 28th days after the onset of ischaemia. Ischaemic animals were treated with naftidrofuryl, 15 mg kg-1 day-1 i.p., from the first to 28th day. 3. Microsphere-embolism caused a sustained decrease in cortical and striatal blood flow over a period of 28 days, whereas hippocampal blood flow was decreased on the 3rd day but not on the 7th or 28th day. On the 3rd day, the striatal and hippocampal but not cortical blood flow of naftidrofuryl-treated, microsphere-embolized rats was higher than untreated rats. On the 7th and 28th days, the cortical and striatal blood flow of the treated and untreated animals did not differ. 4. Brain slices from microsphere-embolized rats contained areas, which were not stained with triphenyltetrazolium chloride (TTC), to a similar degree on the 3rd, 7th and 28th days, indicating the genesis of cerebral infarction. TTC-unstained areas of microsphere-embolized rats that had received naftidrofuryl treatment were smaller than those of untreated rats on the 3rd and 7th days, but not on the 28th day. 5. The results suggest that naftidrofuryl improves cerebral circulation impaired by microsphere-induced ischaemia and this higher level of cerebral blood flow of the treated animal may account for the delayed development of cerebral infarction.
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PMID:Effects of naftidrofuryl oxalate on microsphere embolism-induced decrease in regional blood flow of rat brain. 803 46

The neuroprotective effects of escitalopram oxalate in rats with chronic hypoperfusion and the possible mechanism were explored. Chronic hypoperfusion (2-VO) model was prepared and given escitalopram oxalate (experimental group) or PBS (control group) after 6 weeks. Eight weeks after the operation, Morris water maze test was carried out to evaluate the learning and memory ability of the rats. The cell proliferation, three-dimensional vascular distribution, cell morphological changes in ischemic area and the plasma vascular endothelial growth factor (VEGF) were detected to explore the possible mechanisms. (1) Morris water maze test showed that the escape latency in the experimental group was significantly shorter than in the control group, while the first quadrant swimming time in the experimental group was significantly longer than the control group (both P<0.01). (2) Cerebrovascular confocal detection results showed that the inside diameter of capillaries was significantly less in the experimental group than in the control group; the vascular density was significantly increased in the experimental group and the total area of capillaries was also significantly increased in the experimental group as compared with the control group. (3) There was statistically significant difference in BrdU-positive cells in the ischemic brain tissue between the experimental group and the control group (P=0.003<0.01). (4) VEGF concentrations in the plasma and the ischemic area were higher in the experimental group than in the control group (P<0.05). It was concluded that escitalopram oxalate could significantly improve the learning and memory ability of the rats with chronic cerebral ischemia probably by the VEGF-mediated angiogenesis.
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PMID:Neuroprotective effect of escitalopram oxalate in rats with chronic hypoperfusion. 2622 19