Differential effects of alveolar and arterial oxygen tension on pulmonary vasomotor tone in ECMO-perfused, isolated piglet lungs.

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.