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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of subarachnoid hemorrhage (SAH) on endothelium-dependent vasodilation of isolated rabbit basilar artery was examined using an isometric tension recording method. Thirty-five rabbits that had 2 successive blood injections were divided into 3 groups: normal animals (control), 4 days, and 3 weeks after the first SAH. Acetylcholine (ACh) (10(-6)-10(-4) M) and adenosine triphosphate (ATP) (10(-6)-10(-4) M) were used to evoke dose-dependent vasodilation of isolated arterial rings previously contracted by 10(-6) M serotonin. In the animals killed 4 days after the first SAH, both ACh- and ATP-induced relaxation were suppressed, and the degree of relaxation of this group was 38 +/- 4.5% (mean +/- SEM) and 22 +/- 3.9% of the initial contractile tone in response to 10(-4) M ACh and 10(-4) M ATP, respectively. Suppression of the relaxation induced by ATP was seen even in the animals killed 3 weeks after the first SAH. Moreover, pretreatment with hemoglobin (10(-6) and 10(-5) M) inhibited endothelium-dependent vasodilation induced by ACh in the arterial rings from the animals killed 4 days after the first SAH. The present experiments suggest that impairment of the endothelium-dependent vasodilation following SAH may be involved in the pathogenesis of cerebral vasospasm.
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PMID:Impairment of endothelium-dependent vasodilation induced by acetylcholine and adenosine triphosphate following experimental subarachnoid hemorrhage. 356 7

Experimental delayed cerebral vasospasm was produced in canine basilar arteries by 2 successive injections, 2 days apart, of fresh autogenous arterial blood into the cisterna magna. When angiographic evidence of delayed vasospasm was confirmed 7 days after the initial intracisternal blood injection, a selective inhibitor of 5-lipoxygenase, 2-(12-hydroxydodeca-5,10-diynyl)-3,5,6-trimethyl-1,4-benzoqu inone (AA-861), was infused intravenously at 6.5 X 10(-4) mg/kg/min for 2 hours. However, angiographic evidence of delayed vasospasm was not reversed, and mean regional cerebral blood flow was not significantly increased. In other studies, oral doses of AA-861 at 100 mg/kg/day were given twice a day for 7 days after the initial intracisternal blood injection. In the treated group, angiographic evidence of delayed vasospasm was significantly reduced, and the contractile property of excised basilar arteries in response to vasoconstrictor agents was significantly improved. It is suggested that leukotrienes, 5-lipoxygenase products of arachidonic acid, might be important etiologic factors responsible for the development of delayed vasospasm and that AA-861 would have a therapeutic effect not on the reduction of delayed vasospasm once developed but on the prevention of the development of delayed vasospasm.
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PMID:Effect of 5-lipoxygenase inhibitor on experimental delayed cerebral vasospasm. 356 11

This study examined the role of denervation supersensitivity in the development of cerebral vasospasm. Adrenergic denervation of cat basilar artery was accomplished by resection of the superior cervical ganglia or by injection of 6-hydroxydopamine into the cisterna magna. In vivo dose-response characteristics were determined for normal and for denervated arteries, and no significant differences were found between topical applications of serotonin, norepinephrine, epinephrine, fresh blood, or incubated blood. In addition, analysis of cat blood incubated in vitro revealed that the levels of serotonin, norepinephrine, and epinephrine diminished over time, whereas levels of hemoglobin and methemoglobin increased up to Day 14. The results of this study indicate that adrenergic denervation is not the cause of cerebral vasospasm and that, whatever the mechanism, hemoglobin is far more likely to play a role than are the other agents.
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PMID:Does cerebral vasospasm result from denervation supersensitivity? 381 Jul 75

Cerebral vasospasm following aneurysmal subarachnoid hemorrhage is one of the most important causes of cerebral ischemia, and is the leading cause of death and disability after aneurysm rupture. There are two definitions of cerebral vasospasm: angiographic and clinical. Care must be exercised to be certain that it is clear which entity is being addressed. The diagnosis of the clinical syndrome is one of exclusion and can rarely be made with absolute certainty. The pathogenesis of cerebral vasospasm is poorly understood. Most current theories focus on the release of factors from the subarachnoid clot. More attention must be given to the role of endothelial damage and alterations in the blood-arterial wall barrier. The application of modern techniques for studying vascular smooth muscle which have been developed as a result of research in the areas of hypertension and atherosclerosis must be applied to the problem of cerebral vasospasm. A stress test to select patients with angiographic arterial narrowing who have adequate cerebral vascular reserve to undergo surgery should be developed. The optimal treatment of vasospasm awaits development of agents for blocking or inactivating spasmogenic substances or blocking arterial smooth muscle contraction. Rheological or hemodynamic manipulations to prevent or reverse ischemic consequences of vasospasm are relatively effective, but complicated and hazardous, and should be viewed principally as interim measures awaiting development of more specific therapies for the arterial narrowing.
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PMID:Cerebral vasospasm following aneurysmal subarachnoid hemorrhage. 1110 78

An overview of the possible factors that might contribute to the development of cerebral vasospasm is presented, with particular emphasis on the possibility that spasm arises from a malfunction of the regulatory or contractile processes in smooth muscle cells. This possibility is emphasized because the evidence for cellular damage and the delayed occurrence of vasospasm are suggestive of pathological alteration. Data regarding the development of spasm in vivo has been reviewed and, to the extent possible, correlated with in vitro studies of cerebrovascular smooth muscle contractility. Short-term in vitro studies of normal cerebral arteries may be of little relevance to the prolonged and severe cerebral vasoconstriction that occurs only after a delay of several days from the initial insult.
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PMID:The relevance of in vitro smooth muscle experiments to cerebral vasospasm. 389 90

The effects of Nimodipine on the global and regional cerebral blood flow were studied in 42 patients with cerebrovascular disorders. In 25 patients with focal deficits such as transitory ischemic attack (TIA), prolonged reversible ischemic neurological deficit (PRIND), and minor stroke due to arteriosclerosis, and in eleven patients with cerebral vasospasm after subarachnoid hemorrhage, the cerebral blood flow was measured by 133Xenon inhalation technique 60 min after oral administration of 40, 60, or 80 mg Nimodipine. In 6 patients with vasospasm the effects of Nimodipine i.v. were examined. The result in twelve patients with minor stroke who were only given placebo (lactose; "test-retest") was identical regional (rCBF) and global (CBF) cerebral blood flow before and 60 min after; placebo, blood pressure, and arterial pCO2 remained constant as well. After Nimodipine, however, the CBF increases, the increase after vasospasm being significant when taking the pCO2 in the Wilcoxon test into account. The rCBF increases much more in the regions with low perfusion rates than in well-perfused areas. This is also observed in the patients with TIA, PRIND, or minor stroke, most clearly after oral administration of 60 mg, whereas regions with normal perfusion rates show little reaction. The blood pressure was lowered, depending on the initial pressure. There was no evidence of a steal phenomenon.
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PMID:[Effect of the Ca antagonist nimodipine on global and regional cerebrovascular circulation]. 397 74

The effects of nimodipine, a calcium antagonist with preferential cerebrovascular activity, on the global and regional cerebral blood flow (CBF and rCBF), the intracranial pressure (ICP), and the cerebral perfusion pressure (CPP), were investigated in an acute study. The rCBF of 54 patients was measured by the Xe133 inhalation method under identical conditions before and 60 min after oral administration of nimodipine. 12 patients with focal cerebral circulation disturbances of arteriosclerotic origin, who had suffered a cerebral accident (TIA, PRIND, minor stroke) no more than 3 weeks previously, were given a placebo (test-retest controls) and 25 patients of the same diagnosis and age group were given 40-80 mg nimodipine orally. 11 patients with acute subarachnoid hemorrhage (SAH) from ruptured anterior communicating artery aneurysms and clinical and angiographic signs of vasospasm (Hunt- and Hess grade 3) were likewise treated with nimodipine by the oral route. 6 patients with cerebral vasospasm received nimodipine in i.v. doses of 0.5-2 mg/h. The cerebral blood flow, assessed on the basis of the initial slope index (ISI), before and after the medication, was compared by statistical methods. 12 patients with head injury were given nimodipine intravenously in a dose of 0.5-2 mg with continuous monitoring of the ICP and the blood pressure. The pressure values were evaluated continuously by computer, with calculation of the perfusion pressure, and tested for statistical significance. Oral nimodipine therapy resulted in a significant (14%) increased of the CBF (taking account of the arterial pCO2), the improvement of blood flow being even more pronounced in the hypoperfused regions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute effects of nimodipine on the cerebral blood flow and intracranial pressure. 401 Aug 72

Cerebrovascular and cardiac alterations evoked by intravascular volume expansion with low molecular weight dextran (LMD, molecular weight 40,000), an advocated adjunct in the clinical prevention or therapy of acute stroke and cerebral vasospasm, were studied in splenectomized dogs. Clipping of the right distal internal carotid artery and the proximal middle cerebral artery (MCA) in eight dogs decreased regional cortical blood flow (rCoBF) by 58% without changing cardiac output (CO), and caused 10% +/- 5% (SE) hemispheric infarction. Ten other dogs underwent similar cerebral arterial occlusion and were infused twice with LMD within 2 hours; each infusion equaled 20% of the respective dog's total blood volume. Both CO and rCoBF in the territory of the occluded MCA increased significantly by 119% +/- 13% and 42% +/- 6%, respectively. following the two LMD infusions. Although the mean arterial blood pressure was unaltered, the hematocrit decreased significantly and the intracranial pressure (ICP) increased significantly. The mean hemispheric infarction in these 10 treated dogs was 4% +/- 2%. Another nine dogs underwent arterial manipulation without clipping. Two hemodiluting LMD infusions, similar to those in the 10 dogs, significantly elevated CO and ICP but not rCoBF. These data suggest that hypervolemic hemodilution with LMD effectively elevates collateral perfusion to ischemic regions of brain distal to occluded MCA segments and concomitantly raises the CO and ICP.
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PMID:Hypervolemic hemodilution in experimental focal cerebral ischemia. Elevation of cardiac output, regional cortical blood flow, and ICP after intravascular volume expansion with low molecular weight dextran. 619 56

In helically-cut strips of dog basilar and mesenteric arteries, the isometric tension developed by application of ghost-free hemolysate from dog erythrocytes was recorded. The hemolysate contracted basilar arteries in a concentration-dependent fashion, the response being attenuated by treatment with either aspirin or polyphloretin phosphate, a prostaglandin antagonist. Mesenteric arteries were contracted only slightly by high concentrations of hemolysate. When the mesenteric arteries had partially been contracted with prostaglandin F2 alpha or norepinephrine, the hemolysate induced relaxations, which were abolished by aspirin in approximately half the preparations used. Studies on rat stomach strips exposed to superfusate of dog cerebral arteries showed a release of prostaglandin-like substance by the hemolysate application. It may be concluded that the hemolysate contracts basilar arteries and relaxes mesenteric arteries, mainly through prostaglandins synthesized in and released from the vascular wall. Such a mechanism may be involved in the pathogenesis of cerebral vasospasm following a subarachnoid hemorrhage.
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PMID:Role of intrinsic arachidonate metabolites in the vascular action of erythrocyte breakdown products. 642 Sep 46

The protective properties of PY 108-068 against ischemic disturbances in the brain were investigated in vitro and in vivo. The calcium antagonistic effects were demonstrated on isolated, calcium-loaded arterial rings of feline cerebral arteries. Determination of brain tissue oxygenation with pO2 microelectrodes showed that PY 108-068 improved oxygen supply in the cortex of cats subjected to epicerebral arterial occlusion. In a model of cerebral vasospasm induced by autologous blood superfusion, PY 108-068 reversed the spastic state of cortical microvessels. In a chronic stroke model (microsphere embolization in rats) PY 108-068 led to a significant reduction in mortality and in the severity of neurological symptoms, whereby the peroral efficacy of the drug could be demonstrated. The efficacy of PY 108-068 in a variety of ischemic insults makes this drug a promising aid in the treatment of cerebrovascular accidents.
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PMID:Calcium antagonist PY 108-068: demonstration of its efficacy in various types of experimental brain ischemia. 646 60


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