spasmogenic/acidente vascular cerebral

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Prevention of ventricular fibrillation, acute myocardial infarction (myocardial necrosis), heart failure, and mortality by bretylium: is ischemic heart disease primarily adrenergic cardiovascular disease?

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It is widely, but mistakenly, believed that ischemic heart disease (IsHD) and its complications are the sole and direct result of reduced coronary blood flow by obstructive coronary artery disease (CAD). However, cardiac angina, acute myocardial infarction (AMI), and sudden cardiac death (SCD) occur

Inhibitor of nuclear factor-Kappa B activation attenuates venular constriction, leukocyte rolling-adhesion and microvessel rupture induced by ethanol in intact rat brain microcirculation: relation to ethanol-induced brain injury.

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The present study was designed to test the hypothesis that acute, local administration of a specific inhibitor of nuclear factor-Kappa B activation (which prevents rapid proteolysis of IKB-alpha) will attenuate cerebral (cortical) venular constrictions, leukocyte-endothelial wall interactions and

Antihypertensive profile of cicletanine, a furopyridine derivative: comparison with captopril, indapamide and prazosin.

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The effects of cicletanine were compared with those of three other antihypertensive drugs: prazosin, a highly selective alpha 1 antagonist, captopril an angiotensin converting enzyme inhibitor and indapamide a diuretic antihypertensive agent, on young stroke-prone SHR rats with high salt diet;

Erythropoietin for the treatment of subarachnoid hemorrhage: A feasible ingredient for a successful medical recipe.

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Subarachnoid hemorrhage (SAH) following aneurysm bleeding accounts for 6% to 8% of all cerebrovascular accidents. Although an aneurysm can be effectively managed by surgery or endovascular therapy, delayed cerebral ischemia is diagnosed in a high percentage of patients resulting in significant

Pharmacology of nimodipine, a calcium antagonist with preferential cerebrovascular activity.

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In isolated vessels in vitro nimodipine inhibits spasms induced by depolarization independently of the vessel's origin. The spasms induced by spasmogenic agonists such as serotonin, catecholamines, histamine, thromboxane, or whole blood are inhibited only in the cerebral vessels and not in the

Alcohol-induced vascular damage of brain is ameliorated by administration of magnesium.

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Ethanol ingestion can cause irreversible neuronal and vascular damage in the brain and stroke-like events. Using an intact in vivo rat brain (pial) model, TV image-intensification, cultured cerebral vascular muscle cells, digital-image analysis, and a novel Mg2+ ion-selective electrode to measure

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