Lung fluid exchange after uneven pulmonary artery obstruction in sheep.

Abstract

SUMMARY We studied steady state transvascular fluid and protein exchange after uneven obstruction of the pulmonary arteries. In anesthetized sheep, ventilated by positive pressure, we measured pulmonary artery and left atrial pressures, cardiac output, lung lymph flow, and lymph/plasma protein ratios. We calculated pulmonary vascular resistance. In 16 sheep we obstructed the pulmonary arteries with various microemboli or balloons in lobar arteries until pulmonary vascular resistance was 2-3 times baseline. In every experiment, lung lymph flow increased as pulmonary vascular resistance increased. The lymph/plasma protein ratio did not change. In four sheep, we increased left atrial pressure by balloon obstruction of the mitral orifice. Pulmonary artery pressure increased as much as in the embolization experiments and lymph flow increased but the lymph/plasma protein ratio decreased, meaning that the increased fluid and protein flux after embolization cannot be due to high pulmonary artery or pulmonary venous outflow pressures alone. In four sheep we compared obstruction of the lower lobe pulmonary arteries by balloons with that of upper lobe pulmonary arteries. Lower lobe arterial obstruction caused the lymph flow which drains predominantly from the lower lobes to decrease whereas upper lobe artery obstruction increased lymph flow. This means that the increased fluid and protein flux occurred mainly in the open, perfused portion of the microvascular bed. The mechanism of the increased fluid filtration and protein permeability may be related to high vascular pressure and high linear blood flow velocity through a markedly restricted microvascular bed, although release of substances that affect endothelial permeability is not ruled out.IN THE ADULT respiratory distress syndrome, 1 a central feature is the occurrence of interstitial and alveolar edema. Since in pathological sections the edema fluid stains similarly to blood plasma (proteinaceous) and since there are often hyaline membranes in the air spaces, the edema is considered to be of the increased microvascular permeability variety.2 Hemodynamically, features commonly noted are an increase in pulmonary arterial pressure in the face of a normal pulmonary artery wedge pressure or a directly measured left atrial pressure. The calculated pulmonary vascular resistance is elevated. Numerous investigators 3 " 5 have frequently found plugging of pulmonary small arteries and microvessels by various types of microemboli.How is it that obstruction of pulmonary arteries causes pulmonary edema due to increased microvascular permeability? Gibbon and Gibbon 6 made one of the earliest observations on this syndrome. They found that resection of 70% of the lung mass in cats was followed by the development of pulmonary edema, especially if the resection was accompanied by infusions of whole blood or plasma. Although they believed the edema was due to the high pressure in the microvessels, they did suggest that the edema fluid was only slightly diluted plasma (that is, typical of...

Effects of irradiation on the pulmonary vascular fluid and protein exchange.

“…Since the protein composition of lung lymph is the same as that of free interstitial fluid of the lung (Vreim et al 1976), it is possible to analyze the fluid and protein exchange through the pulmonary vasculature. The elevation of pulmonary microvascular pressure increases the transvascular fluid filtration , and pulmonary microembolism enhances the transvascular fluid and protein permeability (Ohkuda et al 1978). In the present study, irradiation did not affect pulmonary hemodynamics, but increased Qlym and LAP significantly.…”

Polymethylmethacrylate causes prolonged pulmo-nary hypertension during fat embolism: A study in sheep

“…Alternatively, pulmonary vasoconstriction may have been caused by vasoactive cytokines (Malik andvan der Zee 1977, Binder et al 1980). It is unlikely that the increase in PVR was due mechanical occlusion of the pulmonary vessels by emboli or thrombi, because blockage of more than 50% of all pulmonary arteries would be necessary to increase PVR (Dalen et al 1967, Ohkuda et al 1978.…”

Altered lymphatics in an ovine model of congenital heart disease with increased pulmonary blood flow

“…Elegant studies using sheep have previously demonstrated that acute increases in PBF or pressure led to increased capillary filtration of protein-poor fluid and augmented clearance of lymphatic fluid (12,19,42,44,50). However, infants born with congenital cardiac defects often live with increased PBF for months or years before their defects are surgically corrected, and it remains unknown what effect this chronically increased PBF has on the function and structure of the pulmonary lymphatic system.…”