STUDIES ON THE PATHOGENESIS OF AMMONIUM PULMONARY EDEMA

Abstract

Early in ammonium lung edema, there is no great increase, if any, in alveolar capillary permeability. The blood-tinged edema fluid usually seem in the rat and guinea pig is attributed to the fulminating onset and course of lung changes with resultant early capillary anoxia. Anesthetic doses of the central nervous system depressants, pentobarbital, evipal, morphine, chloralose, chlora-losane and ether, did not significantly alter or inhibit the advent of ammonium lung edema. Bilateral adrenalectomy, lateral cervical vagotomy or atropine admn. in doses adequate to block para-sympathetic nerve impulses did not prevent the edema. Evidence for the importance of sympathetic nerve impulses was obtained with dibenamine; this sympatholytic drug prevented ammonium lung edema in most of the animals. Decortication did not prevent the production of lung edema in majority of animals. Surgical de-cerebration prevented this phenomenon while anemic decerebration (two expts.) did not block the lung edema. Low cervical and high thoracic spinal cord transections prevented ammonium pulmonary edema in all animals. Transections between the 3d and 7th thoracic segments prevented it in a minority of the animals. Midlumbar transections did not affect the phenomenon. Division of both sympathetic chains low in the neck did not block the lung edema. The upper thoracic spinal cord must be in functional continuity with the brain stem and it appears that the sympathetic outflow to the thorax, probably the lungs, is necessary in the genesis of this form of pulmonary edema. The site of action of ammonium salts for the production of lung edema appears to be located in the mid- or hindbrain. (The alarm reaction, induced by exposure to cold and to subcut. injn. of formalin, protected most rats from ammonium pulmonary edema.).