Effects of nitroprusside and ketanserin upon pulmonary edema after acid injury

Increased hydrostatic pressure and microvascular permeability after acid aspiration as causes of pulmonary and tracheobronchial edema were studied. Eighteen dogs were anesthetized and 3.0 milliliters per kilogram of 0.1 normal hydrochloride instilled into the trachea. After one hour, the platelet count decreased 47,500 per cubic millimeter (p less than 0.05) from base line levels of 221,400 per cubic millimeter and platelet serotonin stores decreased from 2.09 to 1.65 micrograms per 10(9) platelets (p less than 0.05). Mean pulmonary arterial pressure increased progressively from a base line value of 11 to 21 millimeters of mercury four hours after acid instillation (p less than 0.05). Mean arterial pressure fluctuated from a high of 143 millimeters of mercury to the final value, at four hours, of 119 millimeters of mercury. Ketanserin, a serotonin receptor antagonist, infused one hour after acid injury did not prevent release of platelet 5 hydroxytryptamine but led to a 24 per cent decrease in mean pulmonary arterial pressure from 13 to 10 millimeters of mercury (p less than 0.05) and an 11 per cent decrease in mean arterial pressure from 135 to 120 millimeters of mercury (p less than 0.05). Nitroprusside produced a 30 per cent decrease in mean arterial pressure, but only a 20 per cent decline in mean pulmonary arterial pressure (p less than 0.05). Four hours after acid was instilled, untreated dogs produced 129 milliliters of edema fluid from the endotracheal tube. In proportion to the relative decline in mean pulmonary arterial pressure, nitroprusside therapy reduced the volume of edema to 72 milliliters (p less than 0.05) and ketanserin to 52 milliliters (p less than 0.05). These results suggest that 5 hydroxytryptamine contributes to the pulmonary hypertension associated with acid injury and that the volume of edema formed may be directly related to the increase in the hydrostatic pressure.