IN 1952 Comroe1 implicated serotonin as a possible source of some of the vascular sequelae following pulmonary embolism. He suggested, more specifically,2 that as blood coagulates serotonin is released from the platelets and directly causes bronchoconstriction and pulmonary hypertension. He stated that bradycardia, hypotension, and apnea seem to occur on a reflex basis but attributable to serotonin.
Subsequently, various investigators have reached conflicting conclusions. It is well documented that the intravenous injection or direct injection of serotonin into the pulmonary circulation results in an increase in pulmonary vascular resistance.1-18 Most investigators have stated that this rise in pulmonary vascular resistance is caused by vasoconstriction. Vasoconstriction has been observed to occur in the main pulmonary artery,19 the vessels between the pulmonary artery and arterioles,4 and in the veins.13 Knisely et al20 have obtained evidence by the direct observation of pulmonary vessels that "temporary" embolization