MICROVASCULAR PRESSURES MEASURED BY MICROPIPETTES IN ISOLATED EDEMATOUS RABBIT LUNGS

To study the mechanical effects of lung edema on the pulmonary circulation, we determined the longitudinal distribution of vascular resistance in the arteries, veins, and microvessels, and the distribution of blood flow in isolated blood-perfused rabbit lungs with varying degrees of edema. Active vasomotor changes were eliminated by adding papaverine to the perfusate. In three groups of lungs with either minimal [group I, mean wet-to-dry weight ratio (W/D) = 5.3 .+-. 0.6 (SD), n = 7], moderate (group II, W/D = 8.5 .+-. 1.2, n = 10), or severe (group III, W/D = 9.9 .+-. 1.6, n = 5) edema, we measured by direct micropuncture the pressure in subpleural arterioles and venules (20-60 .mu.m diam) and in the interstitium surrounding these vessels. We also measured pulmonary arterial and left atrial pressures and lung blood flow, and in four additional experiments we used radiolabeled microspheres to determine the distribution of blood flow during mild and severe pulmonary edema. In lungs with little or no edema (group I) we found that 33% of total vascular pressure drop was in arteries, 60% was in microvessels, and 7% was in veins. Moderate edema (group II) had no effect on total vascular resistance or on the vascular pressure profile, but severe edema (group III) did increase vascular resistance without changing the longitudinal distribution of vascular resistance in the subpleural microcirculation. Perivascular interstitial pressure relative to pleural pressure increased from I cmH2O in group I to 2 in group II to 4 in group III lungs. There was an inverse relationship between blood flow and the height of the lung; blood flow was least at the bottom of the lung where edema was greatest. At the top of the lung there was a tendency for blood flow to decrease, probably due to the small increase in interstitial pressure. Decrease in blood flow down the height of the lung may be due to increasing mechanical compression of all vascular segments, or alternatively, due to progressive derecruitment of capillaries.