Galantowicz M E, Price M, Stolar C J
Babies Hospital, Columbia-Presbyterian Medical Center, New York, NY 10032.
J Pediatr Surg. 1991 Mar;26(3):312-5; discussion 315-6. doi: 10.1016/0022-3468(91)90508-q.
Hypoxia is a known stimulant of pulmonary hypertension. We hypothesized graded effects of alveolar (PAO2) and arterial (PaO2) oxygen tension on pulmonary vascular resistance (PVR). A standard in situ, isolated lung preparation was modified by adding an oxygenator to the perfusion circuit with cannulation of the unarrested heart, allowing control of PAO2 and PaO2 in lungs devoid of ischemic injury. Seven anesthetized piglets were prepared with occlusive tracheostomy, ductus arteriosus ligation, and cannulation of the left atrium and main pulmonary artery. Animals were exsanguinated while simultaneously perfusing the lungs with a donor-blood primed extracorporeal membrane oxygenation circuit. Flow, left atrial pressure, pH, and PCO2 were kept constant. PAO2 and PaO2 were altered to establish four different experimental conditions as described by a latin square. PVR was calculated from measurements of pulmonary artery pressure (PAP) before and after introducing an experimental condition. Results show that (1) alveolar hypoxia significantly increases PVR despite arterial hyperoxia; (2) alveolar hypoxia is a more potent stimulus of pulmonary vasoconstriction than arterial hypoxemia; (3) alveolar and arterial oxygen tension are independent, additive effectors of PVR; and (4) recovery from acute hypoxic pulmonary vasoconstriction may be more sensitive to alveolar oxygen tension.
低氧是肺动脉高压已知的刺激因素。我们推测肺泡（PAO2）和动脉（PaO2）氧分压对肺血管阻力（PVR）有分级效应。通过在灌注回路中添加氧合器并对未停跳的心脏进行插管，对标准的原位离体肺制备方法进行了改进，从而能够在无缺血损伤的肺中控制PAO2和PaO2。七只麻醉仔猪进行了闭塞性气管造口术、动脉导管结扎术以及左心房和主肺动脉插管。在通过供体血液预充的体外膜肺氧合回路同时灌注肺的情况下，使动物放血。流量、左心房压力、pH值和PCO2保持恒定。按照拉丁方设计改变PAO2和PaO2，以建立四种不同的实验条件。根据引入实验条件前后肺动脉压力（PAP）的测量值计算PVR。结果表明：（1）尽管动脉血氧过多，但肺泡低氧仍会显著增加PVR；（2）肺泡低氧比动脉低氧血症是更强有力的肺血管收缩刺激因素；（3）肺泡和动脉氧分压是PVR的独立、累加效应器；（4）急性低氧性肺血管收缩的恢复可能对肺泡氧分压更敏感。
