Active and passive components of pulmonary vascular response to vasoactive drugs in the dog

Abstract

Pulmonary blood volume was altered by intravenous infusion of selected drugs. To determine whether these alterations were the result of active changes in pulmonary vascular distensibility or were simply passive, simultaneous hemodynamic measurements were made, including pulmonary blood flow, vascular resistance, and pressures in pulmonary artery, left atrium, small pulmonary veins, and pleural space. In most instances it was necessary to postulate a mixture of active and passive events to account for the results. Epinephrine and norepinephrine elevated left atrial pressure and thus led to passive distention of the pulmonary bed (mean pulmonary blood volume increment, closed chest: epinephrine + 2.6 ml/kg, or 24%; norepinephrine + 2.7 ml/kg, or 25%), in spite of the stiffening and vasoconstrictive effects previously demonstrated in the isolated lung. Isoproterenol increased the volume (+3.4 ml/kg, 31%) and lowered the resistance of the bed by increasing its distensibility, effects sometimes re-enforced by a rise in pressure secondary to increased output. Histamine produced active pulmonary venoconstriction, with passive distention upstream, so that net changes in volume and resistance were variable.