DEPRESSION OF SEROTONIN UPTAKE BY RAT LUNGS EXPOSED TO PARAQUAT

  • 1 January 1982
    • journal article
    • research article
    • Vol. 221  (1) , 254-260
Abstract
Paraquat is a widely used herbicide which causes lung injury in animals and humans. To determine whether pulmonary endothelial cell function is altered during the course of paraquat lung toxicity, serotonin uptake in isolated perfused lungs from rats injected i.p. with 25 mg/kg of paraquat dichloride. In 38 control lungs, serotonin uptake was 0.71 .+-. 0.02 (SE) and was not significantly different in rats studied 4 and 18 h after paraquat administration. In contrast, uptakes were 0.60 .+-. 0.04 (P <.05) 24 h after injection of paraquat. At that time, lung histology and endothelial ultrastructure were unremarkable and dry-to-wet wt ratios of lungs were normal. Forty-eight h after paraquat administration, when light microscope and EM evidence of edema and inflammation were extensive, serotonin uptake was further decreased (P < 0.01). Two wk after injection of paraquat, when fibrosis was present, based on lung histology and hydroxyproline content, serotonin uptakes had returned to control levels. Administration of superoxide dismutase prolonged survival but did not protect against paraquat-induced depression of serotonin uptake. Evidently paraquat causes an early and reversible depression of pulmonary endothelial cell uptake of serotonin which antedates morphological alterations in lung and the endothelial cell and which is not prevented by treatment with exogenous superoxide dismutase. Serotonin uptake may provide a sensitive and specific index of pulmonary endothelial injury.

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