一氧化氮参与低氧脑血管张力调节  

PARTICIPATE OF NITRIC OXIDE PARTICIPATE IN HYPOXIC REGULATION OF CEREBROVASCULAR TENSION

作　　者：顾正中[1] 梅小君[1] 钟凯声[1] 吕敏[1] 

机构地区：[1]中国科学院上海生理研究所

出　　处：《生理学报》1996年第3期222-226,共5页Acta Physiologica Sinica

基　　金：中国科学院上海生理研究所低氧生理开放实验室资助

摘　　要：本工作是在初生小牛基底动脉血管条上，用一氧化氮合成酶（ＮＯＳ）抑制剂─Ｌ－硝基精氨酸（Ｌ－ＮＮＡ）研究ＮＯ及内皮细胞在低氧脑血管扩张机制中的作用。实验结果表明，Ｌ－ＮＮＡ可减弱低氧扩血管作用，但减少的值要小于常氧下相同浓度Ｌ－ＮＮＡ所引起的作用。破坏内皮细胞后，低氧引起的扩血管作用明显小于内皮细胞完整的，其减小的值与Ｌ－ＮＮＡ在低氧下内皮细胞完整时引起的血管张力变化相似。破坏内皮细胞后再给予Ｌ－ＮＮＡ，则对血管张力无明显作用。由此提示，ＮＯ和内皮细胞参与低氧扩血管作用。Making use of nitric oxide synthesase (NOS) inhibitor Nw - nitric - oxide - L-arginine (L-NNA), the effect of NO and the pressence of endothelial cell on hypoxia-induced vascular dilatation was studied with new-born calve basilar artery. The experimental resultsshow that L-NNA can attenuate the hypoxia-induced vascular dilatation, but the magnitude of attenuation is smaller than that of constriction caused by L-NNA on normoxic calve basilar artery. Under hypoxia, the vascular dilatation of endothelial cell denuded artery is smaller than that of endothelial cell intact artery; the difference between them is approximate by the same as the change caused by L-NNA on endothelial call intact artery. After destroying the endothelial cell, L-NNA has no obvious effect on the vascular tension. These results suggest that NO and endothelial cell are involved in hypoxia-induced vascular dilaxation.

关 键 词：脑血管 低氧 一氧化氮 

分 类 号：Q463[生物学—生理学] R331.32[医药卫生—人体生理学]