论文部分内容阅读
目的：探讨大鼠缺氧性肺动脉高压发生过程中肺动脉舒张反应的改变。方法：本实验比较了正常（ｎ＝１１）与慢性缺氧４天（ｎ＝１１）、间断缺氧３周（ｎ＝１１）大鼠离体肺动脉环对几种作用机制不同的血管舒张药物的反应。结果：慢性缺氧显著抑制了大鼠肺动脉环对乙酰胆碱的舒张反应（Ｐ＜０．０５），而对硝普钠（１０－７～１０－１１ｍｏｌ／Ｌ）和硝苯地平（１０－４～１０－８ｍｏｌ／Ｌ）诱发的舒张反应无明显影响；克罗卡林（１０－７～１０－１１ｍｏｌ／Ｌ）在缺氧４天大鼠肺动脉环的舒张作用显著增强（Ｐ＜０．０５）。结论：慢性缺氧显著抑制大鼠肺动脉内皮依赖性舒张反应，而对非内皮依赖性及钙通道依赖性舒张反应无明显影响；钾通道依赖性舒张反应在缺氧早期是增强的
Objective: To investigate the changes of pulmonary vasodilation during hypoxic pulmonary hypertension in rats. Methods: In this study, we compared the effects of isolated pulmonary artery rings on the vasodilator drugs with different mechanisms of action in normal (n = 11) and chronic hypoxia 4 days (n = 11) and intermittent hypoxia for 3 weeks Reaction. RESULTS: Chronic hypoxia significantly inhibited the diastolic response to acetylcholine in rat pulmonary artery rings (P <0.05), but not in sodium nitroprusside (10-7-10-11 mol / L) and nifedipine (10-4 ~ 10-8mol / L) induced no obvious effect on diastolic response. The contractile effect of 10-7 mol·L-1 10-mol / L Cr (superscript 2 +) on the pulmonary artery rings in hypoxia rats increased significantly (P <0.05) . CONCLUSION: Chronic hypoxia significantly inhibits endothelium-dependent vasorelaxation in rat pulmonary arteries and has no effect on non-endothelium-dependent and calcium channel-dependent vasodilation; potassium channel-dependent vasodilation is enhanced early in hypoxia