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)

In the first part of this experiment, the effects of pharmacotherapy on the neurologic consequences of transient global ischemia were examined in Wistar rats. The control and four experimental groups each contained six rats. In comparison to the control group receiving normal saline (NS) solution, in which no rats survived, all rats given naloxone (Nx) (23 mg/kg), superoxide dismutase (SOD) (10,000 U/kg), or allopurinol (APL) (35 mg/kg), 15 minutes before interruption of cerebral blood flow, survived the 20-minute period of global ischemia (p less than 0.01, p less than 0.01, p less than 0.01, respectively). No rat receiving deferoxamine (DEF) (20 mg/kg) survived the same ischemic period. In the second part of the experiment, the arachidonic acid (AA) content of brain samples was determined by gas chromatography and was used as an indicator of cerebral ischemia. Two control and four experimental groups consisted of six rats each. An ischemia control group received NS, whereas experimental groups were given Nx, SOD, APL, or DEF with the same previous dosage schedule. The animals were decapitated 15 minutes after drug infusion and cerebral ischemia was simulated by incubation of the heads in a 37 degrees C water bath for 60 minutes. AA content of ischemic brain treated with NS was markedly elevated (60.0 +/- 24.1 micrograms/gm of brain tissue), whereas in comparison the AA content of brain treated with Nx (5.1 +/- 3.0 micrograms/gm of brain tissue, p less than 0.05), SOD (3.5 +/- 2.7 micrograms/gm of brain tissue, p less than 0.05), or APL (2.9 +/- 1.5 micrograms/gm of brain tissue, p less than 0.05) all demonstrated much lower levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Experimental pharmacologic cerebroprotection. 313 Apr 95

Evaluation of ischemic brain injury in experimental cerebral infarction in gerbils and rats was performed by means of both proton nuclear magnetic resonance imaging ([1H]NMR-CT) and various histochemical analyses. In vivo nuclear magnetic resonance (NMR) imaging was carried out employing saturation recovery, inversion recovery, and spin echo pulse sequences. Spatial resolution of the images was excellent. The ischemic lesions were detected with a remarkable contrast in inversion recovery and spin echo images within a few hours after insult. Those changes in NMR images consistently corresponded with the various retrospective histochemical observations, especially with methods related to brain edema (K+ staining) rather than structural (enzymatic) studies. Calculated T1 and T2 relaxation times indicated the evolution of the edema state in the brain in situ. They correlated excellently with the retrospective water content measurement. As a result, detailed characterization of the edema state induced by cerebral ischemia was possible in vivo using [1H]NMR imaging.
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PMID:Correlations between proton nuclear magnetic resonance imaging and retrospective histochemical images in experimental cerebral infarction. 315 96

The cerebral energy metabolism and brain oedema were investigated in three experimental cerebral ischaemia models using 31P-NMR spectroscopy (MRS) and 1H-NMR imaging (MRI) in the same subject animal. These measurements were performed also in experimental brain oedema models and the findings were compared with each other. 31P-MRS showed an ischaemic pattern in all of the cerebral ischaemia models, that is, ATP and PCr peaks decreased, and the Pi peak increased and shifted to a higher resonant frequency. However, 31P-MRS did not show any remarkable change in the brain oedema models. On the other hand, 1H-MRI clearly demonstrated brain oedema in the brain oedema model. In the cerebral ischaemia models, 1H-MRI findings differed depending upon the type of model, namely the most marked brain oedema was detected in the unilateral middle cerebral arterial occlusion model and no marked change was detected in the temporary four vessel occlusion model. It was thought that this difference depended on the severity of the ischaemic insult. Accordingly, the fundamental pathophysiological problem of cerebral ischaemia was the energy metabolism disturbance with the brain oedema being associated with this disturbance but occurring secondarily. However, in the brain oedema model the main pathological change was the increase in tissue water.
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PMID:Pathophysiological investigation of experimental cerebral ischaemia using in vivo 31P-NMR spectroscopy and 1H-MRI. 321 46

The experiment was carried out on 18 rabbits in two experimental groups. Group I: animals with complete 15-min cerebral ischemia infused with PGI2 for 3 min before, during and for 15-min after ischemia. Group II = control: animals with complete 15 min cerebral ischemia. In both groups, cell nuclei of the adrenal cortex were examined. In the 3rd and 6th h after ischemia numerous vesicular structures, intranuclear filaments and granulofibrillar bodies were found in the nuclei. The vesicular structures were enclosed in a single smooth membrane, some combined with the nuclear envelope, others remained independent. Amassing in karyoplasm of vesicular structures, intranuclear filaments and granulofibrillar bodies probably leads to death of the adrenal cortex cell after complete cerebral ischemia. It is suggested that vesicular structures may form as the result of disturbances in the water-electrolyte exchange between cytoplasm and karyoplasm of adrenal cells. In the experimental conditions, PGI2 did not affect the development of irreversible ultrastructural changes in adrenal cortex cell nuclei after complete prolonged cerebral ischemia.
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PMID:Failure of prostacyclin effect on the reversal of early ultrastructural changes in cell nuclei of adrenal cortex after complete 15-min cerebral ischemia in rabbit. 332 1

This study was carried out with a recently developed model of focal cerebral ischemia in the rat based on the photochemical induction of thrombotic stroke using the dye Rose Bengal. We examined the change in the volume of the lesion and brain water content, in separate groups of rats, at different times (1, 4, 24, 72, and 168 h) after the induction of the ischemic lesion. The volume of ischemic damage increased rapidly between 1 and 24 h after the ischemic insult and decreased between 24 and 168 h. The lesion at 168 h was significantly larger than that following 1 h of ischemia and similar to that obtained at 4 h, suggesting that the maximum extent of tissue damage (without the involvement of significant edema) was reached within the first 4 h in this model. The enlargement of the lesion after 4 h correlated closely with changes in brain water content.
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PMID:Quantitation of photochemically induced focal cerebral ischemia in the rat. 333 8

The relation of brain eicosanoids to progression of cerebral edema was studied in stroke-resistant spontaneously hypertensive rats subjected to incomplete global brain ischemia induced by bilateral occlusion of the common carotid arteries. Thromboxane B2 and 6-keto prostaglandin F1 alpha levels were significantly elevated 5 minutes after reperfusion but returned to control levels by 30 minutes. In contrast, leukotriene C4 levels increased 2 hours after bilateral common carotid artery occlusion and peaked 30 minutes after reperfusion, with higher levels persisting until 60 minutes after reperfusion. Cerebral ischemia was accompanied by cerebral edema early after reperfusion. The edema correlated with increased leukotriene C4 levels. That the increased brain water content was causally related to an increase in leukotriene C4 was supported by results obtained following administration of the 5-lipoxygenase inhibitors ONO-LP-016 and AA-861. Both inhibitors suppressed the increased leukotriene C4 and brain water contents after reperfusion. Our results indicate that leukotriene C4 is closely associated with an induction of ischemic cerebral edema.
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PMID:Brain eicosanoid levels in spontaneously hypertensive rats after ischemia with reperfusion: leukotriene C4 as a possible cause of cerebral edema. 335 24

Edema formation following severe permanent or temporary cerebral ischemia in gerbils with an artificially reduced platelet count was investigated. Acute focal cerebral ischemia was produced by extracranial carotid ligation, and the local cerebral blood flow was estimated using the hydrogen clearance method. Brain tissue water and sodium and potassium contents were taken as indexes of brain edema. The platelet count was reduced in some gerbils by intravenous injection of neuraminidase. After 60 minutes of ischemia, a marked increase in tissue water and sodium contents accompanied by a decrease in potassium content was observed in untreated gerbils. However, gerbils with a reduced platelet count revealed similar but significantly smaller changes in all the measured parameters. Restoration of blood flow after 60 minutes of ischemia resulted in further accumulation of water and sodium and in depletion of potassium in both groups. These changes were significantly smaller in the gerbils with a reduced platelet count. It is concluded that platelets, activated by cerebral ischemia, may be involved in the development of ischemic brain edema in gerbils.
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PMID:Are blood platelets involved in the pathogenesis of ischemic brain edema in gerbils? 336 76

Using two different models of non ischemic and transient cerebral ischemia in SHR, the effect of hyperosmolar solution with intravenous 10% glycerol on serum lipid peroxides, plasma prostaglandins (TXA2, PGI2), brain water content and brain metabolites were studied. Glycerol did not influence the levels of lipid peroxides, plasma prostaglandins and brain water content in the non ischemic rats. In the transient ischemia group, on the other hand, serum lipid peroxides were significantly reduced in the glycerol administrated group. On the study of plasma prostaglandins, there was no difference of TXA2 levels between two groups, but PGI2 levels were significantly increased in the glycerol administrated group. Brain water content was significantly decreased. And on the study of brain metabolites, ATP concentrations remained higher and lactate concentrations were lower in the glycerol administrated group compared with those in the control group. But there was no difference with pyruvate concentrations between two groups, furthermore L/P ratio improved in the glycerol administrated group. Besides the effect on reduction of brain edema as for hyperosmolar solution, glycerol may indicate improvement of ischemic impediments on brain by the action of antioxidation and reinforcement of PGI2.
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PMID:[Effect of glycerol administration on experimental cerebral ischemia--Part 1. Studies on lipid peroxides, prostaglandins, brain edema and brain metabolites]. 337 Jan 71

The relationship of the osmotic pressure gradient between blood and brain, and the development of ischemic brain edema was studied. Focal cerebral ischemia was produced by left middle cerebral artery occlusion in rats. Brain osmolality was determined with a vapor pressure osmometer, brain water content by wet-dry weight, and tissue sodium and potassium contents by flame photometry. Permeability of the BBB was tested by Evans blue. Measurements were made from the ischemic cortex within 14 days of occlusion. Brain osmolality increased from 311 +/- 2 to 329 +/- 2 mOsm/kg by 6 h after occlusion. Serum osmolality did not change significantly. The osmotic gradient between blood and brain peaked at approximately 26 mOsm/kg. Brain osmolality then decreased to 310 +/- 2 mOsm/kg by 12 h after occlusion and remained at about that same level. Water content increased progressively within 1 day of occlusion, then gradually decreased by 14 days. Brain tissue sodium plus potassium content did not increase within 6 h of occlusion, and Evans blue extravasation was not seen within that time. These findings indicate that an osmotic pressure gradient contributes to the formation of edema only during the early stage of cerebral ischemia. Furthermore, the increase in brain osmolality is not related to tissue electrolyte change or BBB disruption to protein.
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PMID:Ischemic brain edema and the osmotic gradient between blood and brain. 339 16

U74006F is a member of a new family of steroid drugs called 21-aminosteroids, which are potent inhibitors of lipid peroxidation with little or no glucocorticoid or mineralocorticoid activity. We investigated the effects of U74006F on the early ionic edema produced by middle cerebral artery occlusion in rats. Intravenous doses of 3 mg/kg U74006F were given 10 minutes and 3 hours after occlusion. Tissue concentrations of Na+, K+, and water at and around the infarct site were measured by atomic absorption spectroscopy and by wet-dry weight measurements 24 hours after occlusion. Compared with vehicle treatment, U74006F treatment reduced brain water entry, Na+ accumulation, K+ loss, and net ion shift by 25-50% in most brain areas sampled in the frontal and parietal cortex. However, reductions of ionic edema were most prominent and reached significance (p less than 0.005, unpaired two-tailed t test) mostly in the frontoparietal and parietal cortex areas adjacent to the infarct site. Our findings suggest that a steroid drug without glucocorticoid or mineralocorticoid activity can reduce edema in cerebral ischemia but that the effects are largely limited to tissues in which collateral blood flow may be present.
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PMID:21-Aminosteroid reduces ion shifts and edema in the rat middle cerebral artery occlusion model of regional ischemia. 340 99


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