THE EFFECT OF CARBON DIOXIDE ON THE PULMONARY CIRCULATION *

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Abstract
It is recognezed that alteration of alveolar O2 tension affects the pulmonary circulation, but the action of CO2 is less well defined. This study was designed to investigate the manner in which these gases regulate pulmonary hemodynamics. In observations on 15 dogs, a lung lobe was isolated so that it could be ventilated and perfused under constant conditions independent of the remaining lung. CO2 and O2 tension were varied as desired in the alveoli and in arterial or venous blood of that lobe. Pressures and gases were measured in conventional fashion on the arterial and venous sides of the isolated lobe circulation. Ventilation of the isolated lobe with 10% CO2 in air increased alveolar and venous PCO2, decreasing the arterial-venous PCO2 difference. Mean arterial pressure increased from control of 21 mm Hg to 27 mm Hg, and calculated vascular resistance increased 50%. Decreasing the arterial-venous O2 difference in the lobe produced an increased arterial pressure and calculated vascular resistance. Perfusion of the lobe with hypoxic, hypercapnic, and hypocapnic blood did not alter hemodynamics if a wide arterial-venous gradient for O2, or CO2 was maintained. The results indicate that a decrease in pulinonary arterial-venous difference for CO2 or O2 initiates locally an increase in pulmonary vascular resistance and pressure. In this way, alteration of alveolar CO2, as well as O2 change, is responsible for shunting blood to better ventilated lung whenever segmental ventilation is insufficient. In generalized hypoventilation, this may contribute to pulmonary hypertension and right ventricular failure.