慢性缺氧对肺动脉增压反应的影响——组胺受体的作用

本实验观察慢性缺氧幼猪(Ch组)和对照组(C组)对急性缺氧的血流动力学反应及组胺H_1、H_2受体阻断剂扑尔敏、甲氰咪呱的作用。急性缺氧可增加肺动脉压(Ppa),Ch组比C组增加明显(前者增加25mmHg、100%;后者增加17mmHg,83.4%)。缺氧时扑尔敏降Ppa的作用亦为Ch组大于C组(Oh组降11mmHg,C组6mmHg)。甲氰咪呱增Ppa的作用两组相近。结果提示:(1)慢性缺氧能增强HPPR;(2)组胺受体参与HPPR调节;(3)慢性缺氧可能使肺动脉H_1受体活性增强,此变化可能与HPPR增强有关。

Effect of chronic hypoxia on hypoxic pulmonary pressor response in young pigs, the role of histamine receptors

The hypoxic pulmonary pressor response (HPPR) was investigated in 10 anesthetized female Landrace swine (3 months) previously exposed to simulated altitude of 4,000m, 8hr/day for 30 days (Ch group). The intensity of HPPR of the Ch group was compared with that of the control group which had been kept in room air (300m) for 30 days (C group). We then challenged the animals with acute hypoxia (4,000m)to determine the response to hypoxia and the effects of histamine antagonists. The pulmonary artery pressures (Ppa) were found increased in both groups during hypoxia. The Ch group exhibited a greater increase in Ppa than the C group did. Chlorpheniramine (CPA) reduced Ppa from 35 to 29mmHg in C group and 44 to 33mmHg in Ch group. Cimetidine (CMT) raised Ppa from 32 to 37mmHg in C group and 43.5 to 49.9mmHg in Ch group. The effect of CPA on Ppa in Ch group was more marked than in C group while CMT had similar effects on both groups. The results support that: (1) chronic hypoxia may exaggerate HPPR; (2) histamine receptors of pulmonary artery may play a role in modulating HPPR. The activity of pulmonary arterial HI-receptor seems to be enhanced by repeated hypoxic exposures. The enhanced activity might be one of the factors which caused the exaggeration of HPPR.