缓激肽
外渗
间隙
医学
血脑屏障
病理
脑动脉
紧密连接
水肿
解剖
麻醉
化学
内科学
受体
中枢神经系统
生物化学
作者
Michael Wahl,Christoph Görlach,Tibor Hortobágyi,Zoltán Benyó
出处
期刊:PubMed
日期:1999-01-01
卷期号:86 (2): 155-60
被引量:17
摘要
All components of an intracerebral kallikrein-kinin system have been described. Thus, bradykinin (BK) acting from the parenchymal side as well as from the blood side may influence cerebral microcirculation. BK is a potent dilator of extra- and intraparenchymal cerebral arteries when acting from the perivascular side. The vasomotor effect of BK is mediated by B2 receptors which appear to be located at the abluminal membrane of the endothelial cell. Signal transmission from the endothelial to the smooth muscle cell is mediated by NO, prostanoids, free radicals or H2O2 depending on the animal species and on the location of the artery. Selective opening of the blood-brain barrier for small tracers (Na+-fluorescein: MW, 376) has been found in cats during cortical superfusion or intraarterial application of BK. This leakage is mediated by B2 receptors located at the luminal and abluminal membrane of the endothelial cells and probably mediated by an opening of tight junctions. Formation of brain edema has been found after ventriculo-cisternal perfusion or interstitial infusion of BK. This can be explained by increase of vascular permeability and cerebral blood flow due to arterial dilatation thus enhancing driving forces for the extravasation. An increase of the BK concentration in the interstitial space of the brain up to concentrations which induce extravasation, dilatation and edema formation has been found under several pathological conditions. Thus, BK may be involved in edema and necrosis formation after cold lesion, concussive brain injury, traumatic spinal cord and ischemic brain injury.
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