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一氧化氮参与低氧脑血管张力调节

顾正中, 梅小君, 钟凯声, 吕敏

(中国科学院上海生理研究所，上海200031)

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一硝基精氨酸(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。
关键词:低氛;脑血管;一级化氮;内皮细胞

关键词： 低氛; 脑血管; 一级化氮; 内皮细胞

PARTICIPATE OF NITRIC OXIDE PARTICIPATE IN HYPOXIC REGULATION OF CEREBROVASCULAR TENSION

GU ZHENG-ZHONG, MEI XIAO-JUN, ZHONG KAI-SHENG , LU MING

Shanghai Institute of Physiology, Chines Academy of Science, Shanghai 200031)

Abstract

Making use of nitric oxide synthesase (NOS) inhibitor N'0-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 results show 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 Qn 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.

Key words: hypoxia;Cerebral vessels;nitric oxide;endothelial cell

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引用本文：

顾正中, 梅小君, 钟凯声, 吕敏. 一氧化氮参与低氧脑血管张力调节[J]. 生理学报 1996; 48 (3): .

GU ZHENG-ZHONG, MEI XIAO-JUN, ZHONG KAI-SHENG , LU MING. PARTICIPATE OF NITRIC OXIDE PARTICIPATE IN HYPOXIC REGULATION OF CEREBROVASCULAR TENSION. Acta Physiol Sin 1996; 48 (3): (in Chinese with English abstract).