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SUBARACHNOID HEMORRHAGE/BRAIN AUTOREGULATORY DYSFUNCTION

蛛网膜下腔出血/大脑自动调节功能障碍

基本信息

批准号：
3450015
负责人：
ROBERT A SOLOMON
金额：
$ 5.46万
依托单位：
COLUMBIA UNIV NEW YORK MORNINGSIDE
依托单位国家：
美国
项目类别：
财政年份：
1986
资助国家：
美国
起止时间：
1986-07-01 至 1989-06-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/3450015
关键词：
autoradiography biological information processing brain metabolism catecholamines central nervous system cerebral hemorrhage cerebral ischemia /hypoxia histology laboratory rat locus coeruleus norepinephrine radioassay radiotracer subarachnoid space sympathetic nervous system vascular endothelium permeability vasospasm

项目摘要

Our specific aims are to demonstrate that a) disturbances in the cerebral microcirculation, unrelated to vasospasm, develop after subarachnoid hemorrhage (SAH) resulting in global reductions of cerebral blood flow (CBF) and metabolism; b) these disturbances are indicative of a disorder in cerebrovascular autoregulation, perhaps contributing to delayed cerebral ischemia; c) these global alterations of CBF and metabolism are induced by hyperactivity of the noradrenergic neurons derived from the locus coeruleus (LC), which projects diffusely to all regions of the central nervous system and have profound effects on regional cerebral metabolism, CBF, vascular permeability, and cerebral autoregulation. Changes in CBF, metabolic activity, cerebrovascular autoregulation, and brain norepinephrine will be quantitated following experimental SAH in rats. These results will be compared in animals with and without prior destruction of the LC. CBF and metabolism will be studied in these animals using a 14C-butanol indicator fractionation technique, and 14C-deoxyglucose autoradiography. Brain tissue catecholamines will be analyzed with a radioenzymatic assay. These studies might be significant in delineating pathophysiological contributions to cerebral ischemia after SAH. The results might suggest new approaches to patients with ruptured intracranial aneurysms.

我们的具体目标是证明：a）与血管痉挛无关脑微循环发展蛛网膜下腔出血（SAH）后，脑血流量（CBF）和代谢的减少; B）这些紊乱表明脑血管自动调节，可能有助于延迟脑缺血; c）CBF的这些整体改变，代谢是由去甲肾上腺素能神经元的过度活跃引起的。来自蓝斑（LC）的神经元，其投射扩散到中枢神经系统的所有区域，对局部脑代谢、CBF、血管渗透性和脑自动调节。 CBF、代谢活动、脑血管自动调节和脑去甲肾上腺素将被定量在大鼠实验性SAH之后。这些结果将在预先破坏和未破坏的动物中进行比较， LC. 将使用以下方法在这些动物中研究CBF和代谢 14 C-丁醇指示剂分馏技术，和 14 C-脱氧葡萄糖放射自显影。脑组织儿茶酚胺将采用放射酶测定法进行分析。这些研究可能对描述脑缺血的病理生理学贡献 SAH。这些结果可能为治疗患有糖尿病的患者提供新的方法。颅内动脉瘤破裂