摘要
我们比较了正常和长期缺氧大鼠肺血管对缓激肽(BK)和血管紧张素I (AI)的反应性;后者有肺动脉高压和肌肉化的肺小动脉。这些肽分别被肺内皮上的血管紧张素转化酶(ACE)灭活和激活。当肺动脉压(Ppa)的变化反映血管阻力的变化时,以恒定的血流速率灌注离体肺。在常氧和缺氧预收缩过程中,得到了对BK (1 ng-10微克)的剂量响应曲线;BK既降低又增加血管阻力,即血管扩张和血管收缩。正常大鼠只在常氧状态下出现收缩,反映出基底血管张力低,而长期缺氧大鼠只出现扩张,反映出基底血管张力高。正常大鼠缺氧时,低剂量引起扩张,高剂量引起收缩;在长期缺氧的大鼠中,也只有扩张比对照组大。使用ace抑制剂卡托普利后,对照组大鼠在常氧和低氧状态下的收缩都明显增大,而长期缺氧大鼠在高剂量的常氧和低氧状态下的收缩则明显增大; oedema often followed. Dose-response curves to AI (1 ng-micrograms) in normoxia showed greatly enhanced pressor responses in chronically hypoxic compared with normal rats, probably attributable to increased sensitivity to angiotensin II (AII) rather than enhanced conversion of AI to AII. Captopril caused a proportionate reduction in responses in both groups of rats.(ABSTRACT TRUNCATED AT 250 WORDS)