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高血压性脑血管疾病中的血管机制。

Vascular mechanisms in hypertensive cerebrovascular disease.

作者信息

Johansson B B

机构信息

Department of Neurology, University of Lund, Sweden.

出版信息

J Cardiovasc Pharmacol. 1992;19 Suppl 3:S11-5.

PMID:1376827
Abstract

Hypertension causes vascular changes of essentially three types: structurally adaptative changes, degenerative alterations unrelated to atherosclerosis, and atherosclerosis. Structural changes result in an increased peripheral resistance, even in the relaxed vascular bed, and a reduced collateral capacity, thus predisposing to ischemia distal to an arterial stenosis/occlusion and to "watershed" infarcts in connection with a drop in blood pressure. Degenerative changes in the small intracerebral arteries can lead to plasma extravasation and focal brain edema, lacunar infarcts, and intracerebral hemorrhages. Hypertension also predisposes to saccular aneurysms and subarachnoid hemorrhages. Finally, atherosclerotic changes including stenoses or occlusions of predominantly extracranial and pial arteries give rise to transitory ischemic attacks and brain infarcts by artery-to-artery embolism or distal hemodynamic perfusion insufficiency.

摘要

高血压主要引发三种血管变化

结构适应性变化、与动脉粥样硬化无关的退行性改变以及动脉粥样硬化。结构变化会导致外周阻力增加,即便在血管床松弛状态下亦是如此,同时侧支循环能力降低,从而使动脉狭窄/闭塞远端易于发生缺血,并在血压下降时引发“分水岭”梗死。脑内小动脉的退行性变化可导致血浆外渗和局灶性脑水肿、腔隙性梗死及脑出血。高血压还易引发囊状动脉瘤和蛛网膜下腔出血。最后,主要累及颅外和软脑膜动脉的动脉粥样硬化性改变,包括狭窄或闭塞,会因动脉到动脉的栓塞或远端血流动力学灌注不足而导致短暂性脑缺血发作和脑梗死。

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