Abstract
Summary
(1) Ammunium salts in toxic doses produced an acute pulmonary edema in the rat, guinea pig and cat. The cat was more refractory to this effect than the rat and guinea pig. The rabbit did not appear to be susceptible to ammonium lung edema. (2) While a number of routes of administration of ammonium chloride were found effective for the production of acute pulmonary edema, the gavage route (0.09-0.15 g per 100 g of body weight) was most dependable for the guinea pig, and the intraperitoneal route (0.04 g per 100 g of body weight) for the rat. (3) The ammonium ion was found to be the agent responsible for the lung edema. Many ammonium salts produced this effect. Acidosis was ruled out as the primary factor, because acidosis produced in other ways did not result in lung edema. (4) The syndrome of ammonium intoxication consisted chiefly of dyspnea. muscle fasciculations and convulsions, terminating in an early acute pulmunary edema. (5) Gross changes at autopsy were limited to the thoracic cavity. They consisted of pulmonary edema and congestion with variable degrees of hemorrhage and moderate dilatation of the right ventricle, right atrium, and entering venae cavae. The microscopic appearance of the lungs was one of edema, congestion and hemorrhage.
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