SALICYLATE PULMONARY-EDEMA - MECHANISM IN SHEEP AND REVIEW OF CLINICAL LITERATURE

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Abstract
Several clinical reports of salicylate-induced pulmonary edema led to an investigation of the mechanism in a chronic unanesthetized sheep preparation. An aspirin-buffer solution was infused i.v. at rates up to 1200 mg of aspirin/h and effects on lung lymph flow and lymph protein concentration were compared with those seen after mechanical elevation of pulmonary vascular pressures. Aspirin had little effect on lung vascular pressures but caused lung lymph flow to increase an average of greater than twice baseline. Because lymph protein concentrations were higher for a given lymph flow with aspirin than during mechanical pressure elevation, lymph protein clearance (lymph flow .times. lymph to plasma protein concentration) increased much more with aspirin. Thus, aspirin appears to cause increased permeability to fluid and protein in the pulmonary vascular bed. Aspirin caused arterial PO2 to decrease from 83 .+-. 3 SE mm Hg to 74 .+-. 3 mm Hg (P < 0.05) and caused postmortem extravascular lung water to increase. These findings are supported by a review of the clinical literature, indicating that salicylate pulmonary edema in humans is noncardiac in origin and may occur at doses considered therapeutic for some diseases as well as after overdose.

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