Effect of free radicals on pulmonary vascular response to acetylcholine

nary vascular response to acetylcholine. J. Appl. Physiol. 71(3): 821~825,1991.-We describe a model of pulmonary endothelial injury caused by electrolysis-generated free radicals. Rabbit lungs were perfused in situ with Krebs solution at 37°C con-taining 30 PM indomethacin. Electrolysis of this solution for 2 min, with a constant DC current of 20 mA, caused pulmonary vasoconstriction during the passage of current and converted subsequent acetylcholine-induced vasodilation to vasocon-striction. Electrolysis also inhibited endothelial-dependent va-sodilation due to the calcium ionophore A23187 but not that due to sodium nitroprusside, suggesting that smooth muscle function was unaltered, while that of the endothelium of the lung is specifically modified by the stimulus. These effects were prevented by a mixture of superoxide dismutase and catalase or by sodium salicylate, which removes hydroxyl radicals from so