Role of serotonin and serotonin antagonist on pulmonary hemodynamics and microcirculation in hemorrhagic shock

Previous studies showed that pulmonary pathological changes after hemorrhagic shock are similar to those after continuous (2 hours) serotonin infusion. Both conditions produce congestive atelectasis, interstitial and intra-alveolar edema and hemorrhage, and red cell aggregation. Studies in 25 dogs compared pulmonary hemodynamics during 2 hours of hemorrhagic hypotension (40 mm. Hg) with methysergide (serotonin antagonist), without methysergide, and with serotonin (75 mcg. per kilogram per minute) alone. During serotonin infusion in normovolemia, both pulmonary artery (PA) and pulmonary vein wedge (PVW) pressure rose. The pulmonary arteriolar and small pulmonary venous (SPV) constriction were statistically and physiologically significant. Pretreatment with methysergide prior to hypovolemia prevented the SPV pressure rise. Lung changes, grossly, microscopically, and by cinemicroscopy, were greatly reduced by administration of methysergide. These results suggest that serotonin—possibly released by the hypoxic intestine, hypoxic brain, or unstable platelets—plays a significant role in the pulmonary changes secondary to hypovolemic hypotension.