PULMONARY VASCULAR RESPONSES TO ALLOXAN

¹ Surgical Cardiopulmonary Laboratory, Tulane University School of Medicine, New Orleans, Louisiana, and the Department of Pathology, University of Arkansas School of Medicine, Little Rock, Arkansas

The pulmonary vasopressor response to alloxan was studied by a technique of pumpperfusing a hemodynamically separated lobar artery at constant flow with aortic or right atrial blood. Intralobar infusion of alloxan (0.5-1.0 g in 4 to 5 minutes) abruptly increases lobar arterial pressure without effecting pressure in the lobar small veins or left atrium and this pressor response persisted for 15 to 20 minutes after completing the infusion. The pressor response was abolished by perfusing the lobe with low molecular weight dextran rather than blood, but not by passing the alloxan-infused blood through the contralateral lung vessels before perfusing it into the separated lobe. Additionally, the response was not found with infusions of alloxan into the left atrium, but did follow similar rapid injections. The data suggest that the pressor response to alloxan is due to activation of pulmonary vasopressor agents from blood and these agents are not inactivated by passage through the lung. Mechanical obstruction from conglutination of blood cells was not found. Alloxan-induced pulmonary edema is not dependent on the pulmonary vasopressor response but apparently is related to capillary endothehial damage. Pulmonary venoconstriction was not observed in these studies.