McMurtry I F, Petrun M D, Reeves J T
Am J Physiol. 1978 Jul;235(1):H104-9. doi: 10.1152/ajpheart.1978.235.1.H104.
We measured pressor responses in blood-perfused lungs from rats kept at low altitude (LA, 1,520 m) and from rats exposed to simulated high altitude (HA, 4-6 wk at 4,270 m) to see if lungs from chronically hypoxic rats were hyper- or hyporeactive to acute airway hypoxia. HA lungs had bigger pressor responses to intra-arterial angiotensin II, prostaglandin F2alpha, and norepinephrine, but smaller responses to airway hypoxia than did LA lungs. The dose-response curve to hypoxia in HA lungs was shifted to the right of that in LA lungs. Thus, HA lungs were hyperreactive to intra-arterial agonists, but were hyporeactive to acute airway hypoxia. In contrast, additional experiments with rats that had been exposed to HA for 5 wk and then returned to LA for 3 days showed that the lungs from such post-HA rats were hyperreactive to acute airway hypoxia. The decreased pressor responsiveness to acute hypoxia in lungs from chronically hypoxic rats could have been due to an increased activity of some endogenous vasodilator or to some abnormality in the mechanism that couples hypoxia to contraction of the vascular smooth muscle.
我们测量了处于低海拔（LA，1520米）的大鼠以及暴露于模拟高海拔（HA，在4270米处4 - 6周）的大鼠血液灌流肺中的升压反应，以观察慢性缺氧大鼠的肺对急性气道缺氧是反应过度还是反应不足。与LA肺相比，HA肺对动脉内注射的血管紧张素II、前列腺素F2α和去甲肾上腺素具有更大的升压反应，但对气道缺氧的反应较小。HA肺中缺氧的剂量 - 反应曲线相较于LA肺向右偏移。因此，HA肺对动脉内激动剂反应过度，但对急性气道缺氧反应不足。相比之下，对暴露于HA 5周然后返回LA 3天的大鼠进行的额外实验表明，此类HA后大鼠的肺对急性气道缺氧反应过度。慢性缺氧大鼠肺对急性缺氧的升压反应性降低可能是由于某些内源性血管舒张剂的活性增加，或者是由于将缺氧与血管平滑肌收缩相偶联的机制存在某些异常。
