Vascular Response in Dog Lung Induced by Alterations in Pulmonary Arterial CO2 Tension and by Acetylcholine

Abstract

Short administrations of high CO2 (15%) in heparinized dog blood caused a predominant reversible decrease in blood outflow from the ventilated and the quiescent isolated perfused dog lung as detd. by thermopile and volumetric flow methods. An initial and a late increase in outflow was sometimes observed. Inflow was also decreased usually following an initial small increase. An attendant increase in lung volume and a concomitant expulsion of intrapuimonary air were attributed to a pooling of blood in the lung because of increased resistance to outflow of blood arising from a constrictive response of effluent vessels, and/or of parenchymal smooth muscle, along with a passive or active dilatation of pulmonary blood reservoirs which encroached upon intrapulomary air vol. The results indicate that high CO2 exerts a differential effect on various parts of the pulmonary vasculature. Acetylcholine caused similar but more abrupt changes. The possible significance of this similarity of CO2 and acetylcholine effects is discussed.