Marshall C, Marshall B E
Circ Res. 1983 Jun;52(6):691-6. doi: 10.1161/01.res.52.6.691.
The purpose of these studies was to evaluate the influence of perfusate oxygen tension on hypoxic pulmonary vasoconstriction and to identify the site at which both alveolar and perfusate gas tensions stimulate hypoxic pulmonary vasoconstriction. Lungs from adult rats were ventilated and perfused in vitro at constant temperature, PCO2, and pH, with a perfusion circuit incorporating a membrane oxygenator that allowed independent control of the alveolar and perfusate gas tensions. Blood flow to the lung was constant (0.06 ml per g body weight per min), and pulmonary vascular resistance was therefore proportional to pulmonary artery pressure. In study 1, the pulmonary artery pressor response to zero or 22 mm Hg alveolar oxygen was measured when the perfusate oxygen tensions were approximately 8, 26, 41, 64, or 128 mm Hg. The pressor response as a percent of the maximum pressure change was progressively reduced as perfusate oxygen tension increased. For alveolar oxygen tension of zero; the pressor response = 128 -39 (Log PPO2) and r = 0.8 (P less than 0.01), the effect of perfusate gas tension on the response to alveolar gas tension of 22 mm Hg was similar. These results demonstrate that the stimulus for hypoxic pulmonary vasoconstriction is a function of both alveolar and perfusate oxygen tension. In study 2, the response to alveolar oxygen tension of 42 mm Hg was measured with mean perfusate oxygen tensions of 130, 52, and 17 mm Hg. In six animals with forward perfusion, the responses decreased with increasing perfusate oxygen tension, as in study 1. In another six animals, with retrograde perfusion, the responses to alveolar hypoxia were not altered when perfusate oxygen tension was increased. These results demonstrate that the sensor region for hypoxic pulmonary vasoconstriction is precapillary. These studies confirm and extend previous hypotheses that alveolar and perfusate oxygen tensions together, determine the PO2 at a precapillary site to stimulate hypoxic pulmonary vasoconstriction.
这些研究的目的是评估灌注液氧分压对低氧性肺血管收缩的影响，并确定肺泡和灌注液气体张力刺激低氧性肺血管收缩的部位。成年大鼠的肺在体外进行恒温、PCO2和pH恒定的通气和灌注，灌注回路包含一个膜式氧合器，可独立控制肺泡和灌注液气体张力。肺血流量恒定（每分钟每克体重0.06毫升），因此肺血管阻力与肺动脉压成正比。在研究1中，当灌注液氧分压分别约为8、26、41、64或128毫米汞柱时，测量肺动脉对零或22毫米汞柱肺泡氧的升压反应。随着灌注液氧分压升高，作为最大压力变化百分比的升压反应逐渐降低。对于肺泡氧分压为零时，升压反应=128 - 39（Log PPO2）且r = 0.8（P小于0.01），灌注液气体张力对22毫米汞柱肺泡气体张力反应的影响相似。这些结果表明，低氧性肺血管收缩的刺激因素是肺泡和灌注液氧分压的函数。在研究2中，测量了平均灌注液氧分压为130、52和17毫米汞柱时对42毫米汞柱肺泡氧的反应。在六只进行顺行灌注的动物中，反应随灌注液氧分压升高而降低，与研究1相同。在另外六只进行逆行灌注的动物中，当灌注液氧分压升高时，对肺泡缺氧的反应未改变。这些结果表明，低氧性肺血管收缩的感受器区域位于毛细血管前。这些研究证实并扩展了先前的假设，即肺泡和灌注液氧分压共同决定毛细血管前部位的PO2以刺激低氧性肺血管收缩。
