Heistad D D, Baumbach G L
Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242.
J Hypertens Suppl. 1992 Dec;10(7):S71-5.
To examine new concepts concerning structural changes in cerebral blood vessels during chronic hypertension, and to examine mechanisms that lead to cerebral vascular complications, in light of the hypothesis that hypertensive vascular hypertrophy may be harmful.
Literature review.
The evidence suggests that the current view is not correct in relation to the cerebral circulation. Vascular hypertrophy and remodeling appear to protect cerebral vessels during hypertension, instead of being harmful. Major cerebral vascular complications during hypertension may be largely due to endothelial dysfunction. One function of the cerebral endothelium is to serve as the blood-brain barrier. Disruption of the blood-brain barrier appears to mediate hypertensive encephalopathy. A second endothelial function is to modulate vascular tone. Abnormalities in vasoactive factors that are released by the endothelium (impaired vasodilator mechanisms and augmented vasoconstrictor mechanisms) may make an important contribution to the pathophysiology of transient ischemic episodes, and perhaps stroke, in chronic hypertension.
鉴于高血压性血管肥大可能有害这一假说,研究慢性高血压期间脑血管结构变化的新概念,并研究导致脑血管并发症的机制。
文献综述。
有证据表明,目前关于脑循环的观点并不正确。血管肥大和重塑在高血压期间似乎对脑血管起到保护作用,而非有害。高血压期间主要的脑血管并发症可能很大程度上归因于内皮功能障碍。脑内皮的一项功能是充当血脑屏障。血脑屏障的破坏似乎介导了高血压脑病。内皮的第二项功能是调节血管张力。内皮释放的血管活性因子异常(血管舒张机制受损和血管收缩机制增强)可能对慢性高血压中短暂性缺血发作以及可能的中风的病理生理学起到重要作用。