Role of platelets in the acute pulmonary responses to endotoxin.

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Abstract
The injection of bacterial endotoxin in dogs resulted in rapid changes in lung mechanics, indicative of airway constriction. The prior injection of heparin, the concurrent administration of a serotonin antagonist, or the induction of severe thrombocytopenia prevented endotoxin from inducing airway constriction. The acute changes in lung mechanics observed following endotoxin are believed to result from the release of serotonin from platelet aggre-gates. The similarity of the acute changes in lung mechanics fol-lowing autologous massive thromboemboli and platelet aggregates acting as microemboli suggests that, in both, serotonin release with subsequent contraction of small airways is primarily responsible for the changes observed. In contrast to the changes after massive thromboemboli, increases in arterial-alveolar PCO2 [carbon dioxide pressure] difference and marked decreases in arterial oxygen tension were unusual after microemboli. Although localized changes in alveolar ventilation and pulmonary capillary perfusion undoubtedly occur, it is likely that the alveolar ventilation/perfusion relationships of the gas exchange units remain near preembolic levels following this type of microembolism.