Microvascular occlusion by platelet emboli after transfusion and shock

Abstract

Following hemorrhagic shock and transfusions of stored blood in anesthetized dogs, we observed increases in the arterial-alveolar carbon dioxide tension difference (indicating an increase in alveolar dead space) and gross hemorrhages in the lungs (at subsequent autopsy). The increase in alveolar dead space constitutes an evidence of regional pulmonary vascular obstruction which is correlated with an increase in platelet adhesiveness/aggregation as measured by the screen filtration pressure. When heparin was administered during hemorrhagic shock, the increase in alveolar dead space and the post-mortem hemorrhage was lessened. When a serotonin antagonist was administered during hemorrhagic shock, the increase in alveolar dead space and post-mortem hemorrhage was abolished. Regional pulmonary vascular obstruction caused by platelet aggregates and perhaps enlarged by fibrin during shock is probably due in large part to the action of serotonin.