In vivo studies of pial vascular permeability to sodium fluorescein: absence of alterations by bradykinin, histamine, serotonin, or arachidonic acid.
In vivo studies of pial vascular permeability to sodium fluorescein: absence of alterations by bradykinin, histamine, serotonin, or arachidonic acid.
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软脑膜血管对荧光素钠通透性的体内研究：不存在缓激肽、组胺、血清素或花生四烯酸的改变。
DOI：
10.1161/01.str.18.6.1157
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发表时间：
1987
期刊：
影响因子：
8.3
通讯作者：
Rosenblum,WI
中科院分区：
文献类型：
--
作者：
Watanabe,M;Rosenblum,WI
我们在小鼠体内研究了脑脊液血管，在汞灯下检测了这些血管对荧光素钠的渗透性。局部应用高渗氯化钠溶液引起荧光素渗漏。然而，假定的渗漏化学介质，如组胺、血清素、花生四烯酸和缓激肽，都不能增加对染料的渗透性。通透性的明显增加仅伴随染料+光组合引起的内皮损伤，如局部血小板聚集物的产生所示。如果能识别并避免无意的内皮损伤，该技术是有用的。小鼠的数据表明，我们所测试的几种介质在脑实质血管中产生的通透性变化可能不参与脑实质血管的通透性变化。因此，对枕部血管通透性的研究不能为可能介导脑水肿的药物的作用提供可靠的数据。
We studied pial vessels in vivo in mice, examining under mercury light the permeability of these vessels to sodium fluorescein. Topical application of hypertonic solutions of NaCl caused leakage of fluorescein. However, putative chemical mediators of leakage, such as histamine, serotonin, arachidonic acid, and bradykinin, all failed to increase permeability to the dye. Apparent increases in permeability only accompanied endothelial damage caused by the dye + light combination, as indicated by production of local platelet aggregates. The technique is useful, provided inadvertent endothelial injury is recognized and avoided. The data in mice suggest that pial vessels may not participate in the permeability changes reportedly produced in parenchymal brain vessels by several of the mediators we tested. Therefore, studies of pial vascular permeability are not expected to provide reliable data concerning the actions of agents that might mediate cerebral edema.