Beta-adrenergic modulation of pulmonary transvascular fluid and protein exchange

Publisher Website
Google Scholar
Abstract
We determined in anesthetized sheep whether isoproterenol, a .beta.-adrenergic agonist, prevents the increases in pulmonary fluid and protein exchange produced by thrombin-induced intravascular coagulation. Seven sheep were infused intravenously with 0.05 .mu.g .cntdot. kg-1 .cntdot. min-1 isoproterenol before infusion of .alpha.-thrombin, and six sheep were infused with .alpha.-thrombin only and served as control subjects. The marked increases in pulmonary lymph flow and lymph protein clearance in the control thrombin group were attenuated (P < 0.05) in the isoproterenol group in association with a higher pulmonary blood flow (P < 0.05) and a lower pulmonary vascular resistance (P < 0.05) in the isoproterenol group and with similar increases in pulmonary arterial and pulmonary arterial wedge pressures in both groups. The decreases in fluid and protein fluxes produced by isoproterenol are related to its .beta.-adrenergic properties because propranolol, a .beta.-adrenergic antagonist, blocked the protective effects of isoproterenol in a second group of sheep infused with propranolol, isoproterenol, and thrombin. Raising left atrial pressure to test for changes in vascular permeability increased protein flux to a much greater extent in the thrombin control group than in the isoproterenol group challenged with thrombin. The data suggest that isoproterenol attenuated the increase in fluid and protein fluxes produced by thrombin-induced intravascular coagulation by a permeability-decreasing mechanism.