Pulmonary vascular effects of serotonin (5-OH-tryptamine) in dogs: its role in causing pulmonary edema

Abstract

Rapid injection of serotonin (0.5–6.5 mg) was made into the pulmonary artery in 22 experiments in 12 open-chest anesthetized dogs. Serotonin caused pulmonary arteriolar and venous constriction in the majority of experiments, shown by an increase in the pressure gradients between the pulmonary artery and pulmonary artery wedge pressures, and between the latter and the left atrial pressure, respectively. Three groups of responses were obtained as far as the production of pulmonary edema is concerned. The first group (3 dogs) showed no pulmonary edema. The second (group II—6 dogs) showed moderate to severe bilateral pulmonary edema without evidence of left heart failure. The third (3 dogs) also showed severe bilateral pulmonary edema but in the presence of left heart failure. In group II, the evidence suggests that an increase in capillary permeability is responsible, at least in part, for the pulmonary edema found. The similarity of results in group II to those obtained in the formation of bilateral pulmonary edema following unilateral starch embolization, suggests that serotonin could be the initiating factor in the neurohumoral mechanisms involved—or one of them.