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To determine the lung microvascular pressure profile during hypoxia, we micropunctured the subpleural microcirculation of isolated perfused cat lungs. Our procedures involved exsanguinating a cat, then cannulating its pulmonary artery, left atrium, and trachea. Using the cat's own blood, we perfused the lungs at pulmonary artery and left atrial pressures of 18 and 9 cm water, respectively, to obtain lung blood flow of 81 +/- 29 ml/(kg body weight x min), which we held constant throughout the experiment. We stabilized the lung surface with a vacuum ring and micropunctured 30- to 50-micrometers arterioles and venules to measure microvascular pressure by the servo-null method. During micropuncture, we held the lungs at constant inflation using airway pressure of 8 cm water. We varied the oxygen concentration of the inflation gas from 30% during baseline to 2% during hypoxia. We studied groups with high (more than 7.5) or normal pH. During normoxia, 27, 44, and 29% of the pressure drop occurred in the arterial, capillary and venous segments, respectively. During hypoxia, the increase in pulmonary vascular resistance, which was marked in both groups, was significantly greater in the normal pH group. All segmental pressure drops increased significantly during hypoxia. However, the predominant increase occurred in the arteries where segmental pressure drop increased by 148% and 210%, respectively, in the high and normal pH groups. We conclude that the major site of hypoxic vasoconstriction is in the pulmonary arteries.

We punctured subpleural microvessels in 19 isolated blood-perfused dog lung lobes to determine the effect of 5-hydroxytryptamine (5-HT) on the pulmonary microvascular pressure profile. Maintaining lobe airway pressure at 6 cmH2O and lobe venous pressure at 10 cmH2O we infused saline alone (10 microliter/min) in 10 control lobes and 5-HT in saline solution (100--150 micrograms/min) in 9 lobes. We measured pressures in subpleural microvessels using micropipettes connected to a servo-null system. The 5-HT infusion doubled lobar vascular resistance. In all microvessels upstream from the 150-micrometer venules, pressure was higher than in the control lobes. In contrast to the control lobes, pressure dropped markedly from the lobar artery to the 50-micrometer arterioles and from the venous capillaries to the 50-micrometer venules. We conclude that 5-HT not only constricted arterioles, but also raised lung microvascular pressure by constricting postcapillary venules.

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