Welling K L, Sanchez R, Ravn J B, Larsen B, Amtorp O
Department of Cardiology, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark.
J Appl Physiol (1985). 1993 Sep;75(3):1194-200. doi: 10.1152/jappl.1993.75.3.1194.
The time course of hypoxic pulmonary vasoconstriction and its segmental distribution were studied during prolonged (150 min) alveolar hypoxia in in vivo dog lungs at constant-flow perfusion. With the pulmonary and the systemic circulations separated by two extracorporeal circuits, adequate systemic oxygenation was achieved throughout the experiments. The pulmonary circulation exhibited a time-related biphasic hypoxic vasoconstrictor response: an initial rapid contraction [79 +/- 11% (SE) above control level] was followed by a partial relaxation when a second slow and sustained vasoconstriction (92 +/- 13% above control level) superseded. We partitioned the pulmonary circulation into two segments by arterial occlusion: an upstream arterial segment and a downstream segment consisting of a middle and a venous segment. Measurements were performed at baseline and during the late sustained vasoconstrictor response. Prolonged alveolar hypoxia increased pulmonary capillary pressure by 90 +/- 18%, the site of pulmonary vasomotion being the arterial upstream and downstream middle and venous segments.
在恒流灌注的犬活体肺中，研究了长时间（150分钟）肺泡缺氧期间缺氧性肺血管收缩的时程及其节段分布。通过两个体外循环将肺循环和体循环分开，在整个实验过程中实现了充分的体循环氧合。肺循环表现出与时间相关的双相缺氧性血管收缩反应：最初是快速收缩[比对照水平高79±11%（标准误）]，随后是部分舒张，此时第二次缓慢且持续的血管收缩（比对照水平高92±13%）取而代之。我们通过动脉闭塞将肺循环分为两个节段：上游动脉节段和由中间节段及静脉节段组成的下游节段。在基线和晚期持续血管收缩反应期间进行测量。长时间肺泡缺氧使肺毛细血管压力升高90±18%，肺血管运动部位为动脉上游、下游中间和静脉节段。
