摘要
利用大鼠颅骨开窗观察软脑膜微循环的方法研究了内皮素１（ＥＴ－１）０．１－１００ｎｍｏｌ·Ｌ－１对正常大鼠软脑膜微循环的影响，失血性休克大鼠软脑膜血管对ＥＴ～１１００ｎｍｏｌ·Ｌ－１的反应性及尼莫地平，川芎嗪，山莨菪碱对ＥＴ－１引起血管痉挛的对抗作用。结果表明，１，１０和１００ｎｍｏｌ·Ｌ－１ＥＴ－１可使正常动物软脑膜小动脉，细动脉强烈收缩，血管收缩率分别为２７％。４７％和７８％、其收缩的强度依赖于ＥＴ－１的浓度、对静脉的作用不明显。０．１ｎｍｏｌ·Ｌ－１ＥＴ－１可使细动脉轻度扩张。出血性休克时，软脑膜血管血流明显减慢、小动脉细动脉对ＥＴ－１的收缩作用更敏感。１００ｎｍｏｌ·Ｌ－１的ＥＴ－１可使细动脉管腔完全关闭，使脑组织血流明显减少尼莫地平具有较好的拮抗ＥＴ－１引起软脑膜的收缩作用，并使局部血流量增加，改善局部微循环。川芎嗪也能拮抗ＥＴ－１引起软脑膜的动脉收缩，但作用较尼莫地平弱。山莨菪碱不能缓解ＥＴ－１对软脑膜动脉的收缩作用。
The purpose of this study was to de-termine responses of rat cerebral microcirculation toendothelin I(ET-1)and influence of tetramethylpyrazine (TMP), nimodipine and anisodamine oneerebral vasospasm induced by ET-1.In normal rat,topical application of ET-1 produced mild increase inrat arteriole diameter at the lowest concentration (0.1nmol·L-1, 9±s 4%) and coneentrationdependentdecrease in rat arteriole diameter at higher concentra-tion (27±s 4%,47±s 5 % and 78 ± s 5 % at 1.10 and100 nmol·L-1 respectively). While rat was inhemorrhagic shock, due to decrease in blood volume ofbrain tissue, sensitivity of cerebral vasculature to ET-1was increased.Topical application of ET-1 100nmol·L- 1 could result in profound constriction ofcer-ebral arterioles. Diameter of artenole was decreased by-93%.TMP and nimodipine could attenuate constric-tion induced by ET-1. Muscarinic receptor blockeranisodamine did not affect the action of ET-1.Theseresults suggested that ET- 1 may play an importantrole in the pathogenesis of ischemic cerebral vasculardiseases.Antagonistic action of TMP may account forthe mechanism of TMP in treating cerebral ischemia.
出处
《中国药理学与毒理学杂志》
CSCD
北大核心
1994年第3期175-178,共4页
Chinese Journal of Pharmacology and Toxicology
关键词
血管收缩药
血管扩张药
内皮素
vasoconstnctors
vasodilators
endothelin-1
tetramethylpyrazine
nimodipine
shock
hemorrhagic
cerebrovascular circulation
