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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。
This work is in the primary calf basilar artery strips, with nitric oxide synthase (NOS) inhibitor ─ L-nitroarginine (L-NNA) study of NO and endothelial cells in hypoxic cerebral vasodilation mechanism Role. The experimental results show that L-NNA can reduce the hypoxia vasodilator effect, but the decrease is less than the same concentration of normal L-NNA caused by the role. Vasoconstriction induced by hypoxia was significantly less than that of endothelial cells after vasoconstriction, and its decrease was similar to that of L-NNA induced by endothelial cells under hypoxia. Destruction of endothelial cells and then given L-NNA, no significant effect on vascular tone. This suggests that NO and endothelial cells involved in hypoxia vasodilator effect.