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[高血压脑病发病机制的实验数据]

[Experimental data on the pathogenesis of hypertensive encephalopathy].

作者信息

Auer L M

出版信息

Fortschr Med. 1979 Nov 15;97(43):1996-8.

PMID:511079
Abstract

Experimental investigations of the pial vessels during acutely drug-induced hypertension revealed diffuse or sausage-like distension of arterioles. Degree and type of reactions depended on blood pressure characteristics like steepness of increase, percentual increase, duration and peak value in this order. Such vasodistension is interpreted as mechanical overwhelming of smooth muscle force within the arteriolar wall during acute increase of intraluminal pressure. Clinical consequences of these results are: Vasodilators as well as sedatives with respiratory depression are contraindicated for patients with hypertensive crises. Data also make readily apparent, that short lasting acute hypertension may be fatal for patients with preexisting disturbances of blood-brain barrier function as it accelerates the development of brain edema.

摘要

对急性药物性高血压期间软脑膜血管的实验研究显示小动脉呈弥漫性或腊肠样扩张。反应的程度和类型依次取决于血压特征,如升高的陡度、百分比增加、持续时间和峰值。这种血管扩张被解释为管腔内压力急性升高期间小动脉壁内平滑肌力量的机械性压倒性作用。这些结果的临床意义在于:血管扩张剂以及具有呼吸抑制作用的镇静剂对高血压危象患者是禁忌的。数据还很明显地表明,短暂的急性高血压对已有血脑屏障功能障碍的患者可能是致命的,因为它会加速脑水肿的发展。

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