Morphometric and physiological studies of alveolar microvessels in dog lungs in vivo after sustained increases in pulmonary microvascular pressures and after sustained decreases in plasma oncotic pressures

Previous investigations from this laboratory of isolated-perfused dog lungs have shown that volume densities of vesicles in both capillary endothelial and type I epithelial cells are substantially increased after acute, severe edema produced by increasing microvascular pressures (D. O. DeFouw and P. B. Berendsen, 1978, Circ. Res. 43, 72-82) and after decreasing macromolecular concentrations of the perfusate (D. O. DeFouw and P. B. Berendsen, 1979, Microvasc. Res. 17, 90-103). The present study provides morphometric evaluations of alveolar vessel endothelium of the lungs of intact dogs after episodes of sustained increased microvascular pressures and after sustained decreases of plasma oncotic pressures. Endothelial vesicular volume densities did not increase in either case. Fluid accumulation was found in the extraalveolar connective tissue spaces (mainly perivascular); no changes of endothelial or interstitial compartmental thicknesses were observed on either the thin or thick sides of the alveolar septa. Thus, if the increased outward filtration to be expected from the increased hydrostatic or decreased oncotic pressures occurred in the microvasculature, it was moderated by increased hydrostatic and decreased oncotic pressures in the tissues or was accommodated by increased lymph flow rates. Our tentative hypothesis that increased septal interstitial pressure plays a role in initiating vesicle formation in alveolar endothelial cells is consistent with these data if the postulated increases of tissue pressure are less than in the isolated perfused preparations. Our data do not provide support for the concept that endothelial vesicles play a major, early role in the development of pulmonary edema.