Influence of bronchial arterial PO2 on pulmonary vascular resistance.
Influence of bronchial arterial PO2 on pulmonary vascular resistance.
复制标题
支气管动脉PO2对肺血管阻力的影响。
DOI：
10.1152/jappl.1991.70.1.405
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Pietra,GG
中科院分区：
文献类型：
--
作者：
Marshall,BE;Marshall,C;Magno,M;Lilagan,P;Pietra,GG
在6只麻醉和机械通气的成年绵羊身上，将氧气泵回路中的血液注入支气管动脉。当呼吸100%氧气，且肺内氧分压(PbrO2)约为600Torr时，实验开始时(3.32±0.29单位)和结束时(3.17±0.13单位)测得的肺血管阻力(PVR)平均值为3.24±0.20单位。当PbrO2改变为58+/-1Torr时，PVR(2.99+/-0.14个单位)没有明显变化。当PbrO2降至91+/-4、77+/-3、56+/-2和42+/-1Torr时，肺的PVR分别增加到3.67+/-0.18、4.03+/-0.16、4.79+/-0.19和4.71+/-0.35个单位。而当PbrO2进一步降至26+/-1和13+/-1Torr时，PVR分别降至3.77+/-0.28和3.91+/-0.30个单位。相反，随着PbrO2的降低，支气管血管阻力单调降低。支气管循环为除最小的肺动脉外的所有动脉壁供应血管，因此提示，在中度低氧血症时刺激缺氧性肺血管收缩，而在重度低氧血症时刺激低氧性肺血管扩张，支气管循环中的PO2对肺血管系统的双峰反应起作用。讨论了全身性PO2对肺血管张力影响的生理和病理生理学意义。
In six anesthetized and mechanically ventilated adult sheep, the bronchial artery was perfused with blood from an oxygenator-pump circuit. When the lungs were ventilated with 100% O2 and the bronchial O2 tension (PbrO2) was approximately 600 Torr, the mean of the pulmonary vascular resistances (PVR) measured at the beginning (3.32 +/- 0.29 units) and end (3.17 +/- 0.13 units) of the experiment was 3.24 +/- 0.20 units. When the PbrO2 was changed to 58 +/- 1 Torr, the PVR (2.99 +/- 0.14 units) did not change significantly. However, when the lungs were ventilated with air as PbrO2 was decreased to 91 +/- 4, 77 +/- 3, 56 +/- 2, and 42 +/- 1 Torr, the PVR increased to 3.67 +/- 0.18, 4.03 +/- 0.16, 4.79 +/- 0.19, and 4.71 +/- 0.35 units, respectively. However, when the PbrO2 was decreased further to 26 +/- 1 and 13 +/- 1 Torr, the PVR decreased to 3.77 +/- 0.28 and 3.91 +/- 0.30 units, respectively. In contrast, the bronchial vascular resistance decreased monotonically as PbrO2 decreased. The bronchial circulation supplies vasa vasorum to the walls of all but the smallest pulmonary arteries, and it is therefore suggested that the PO2 of the bronchial circulation is responsible for the bimodal response of the pulmonary vasculature, with stimulation of hypoxic pulmonary vasoconstriction at moderate hypoxemia and of hypoxic pulmonary vasodilation at profound hypoxemia. The physiological and pathophysiological significance of the influence of systemic PO2 on pulmonary vascular tone is discussed.