STIMULATION OF LUNG EPITHELIAL LIQUID CLEARANCE BY ENDOGENOUS RELEASEOF CATECHOLAMINES IN SEPTIC SHOCK IN ANESTHETIZED RATS

Exogenous administration of beta-adrenergic agonists has previously be en reported to increase lung liquid clearance by stimulation of active sodium transport across the alveolar epithelium. We hypothetized for this study that endogenous release of epinephrine in septic shock woul d stimulate liquid clearance from the airspaces in rats. Liquid cleara nce from the air spaces was measured by the concentration of protein o ver 4 h in a test solution of 5% albumin instilled into one lung. Bact eremic rats developed severe systemic hypotension and metabolic acidos is that was associated with a 100-fold rise in plasma epinephrine leve ls. There was a 100% increase in liquid clearance from the airspaces o f the lung in the bacteremic compared with control rats. To determine the mechanisms responsible for this accelerated lung liquid clearance, amiloride (10(-3) M), a sodium transport inhibitor, was added to the air spaces. Amiloride prevented the increase in liquid clearance from the airspaces, indicating that this effect depended on increased uptak e of sodium across the lung epithelium. The addition of propranolol (1 0(-4) or 10(-5) M) to the instillate also prevented the acceleration i n alveolar liquid clearance in the bacteremic rats. We conclude that t he release of endogenous catecholamines associated with septic shock m arkedly stimulates fluid clearance from the distal airspaces of the lu ng by a beta-adrenergic mediated stimulation of active sodium transpor t across the epithelial barrier. This data provides evidence for a pre viously unrecognized mechanism that can protect against or hasten the resolution of alveolar edema in pathological conditions, such as septi c shock, that are associated with the endogenous release of catecholam ines.