Benumof J L, Wahrenbrock E A
J Appl Physiol. 1975 May;38(5):846-50. doi: 10.1152/jappl.1975.38.5.846.
We tested the hypothesis that increased pressures within the lung vessels would inhibit hypoxic pulmonary vasoconstriction at all levels of alveolar CO2 tension. Selective hypoxia of the left lower lobe of the lung in open chested dogs caused the electromagnetically measured blood flow to the lobe to decrease 51 plus or minus 4 (SE) percent and its vascular resistance to increase 132 plus or minus 13 percent. Pressure and blood flow in the main pulmonary artery and left atrial pressure did not change during the hypoxic response. Stepwise increments in left artrial and pulmonary arterial pressures induced either by inflating a left atrial balloon or infusing dextran, progressively diminished the vasoconstrictive response to hypoxia. The response was usually abolished when left atrial pressure reached 25 mmHg. For all vascular pressures, hypoxic vasoconstriction was blunted by hypocapnic alkalosis but not enhanced by hypercapnia. We conclude that the redistribution of blood flow away from an hypoxic lobe of the lung to lobes with high Po2 was greatly attenuated by increasing pressures within lung vessels or by inducing respiratory alkalosis.
在所有肺泡二氧化碳张力水平下,肺血管内压力升高会抑制低氧性肺血管收缩。在开胸犬中,对左下肺叶进行选择性低氧处理,导致通过电磁测量的该肺叶血流量减少51±4(标准误)%,其血管阻力增加132±13%。在低氧反应过程中,主肺动脉压力、血流量以及左心房压力均未发生变化。通过向左心房球囊充气或输注右旋糖酐诱导左心房和肺动脉压力逐步升高,逐渐减弱了对低氧的血管收缩反应。当左心房压力达到25 mmHg时,该反应通常会消失。对于所有血管压力而言,低氧性血管收缩在低碳酸血症性碱中毒时会减弱,但在高碳酸血症时不会增强。我们得出结论,通过增加肺血管内压力或诱导呼吸性碱中毒,可使血液从低氧肺叶重新分布到高氧肺叶的情况大大减弱。