We examined pulmonary gas exchange in 19 anesthetized dogs during the induction of acute pulmonary edema by intravenous infusion of dextran in saline. We monitored pulmonary capillary pressure by a left atrial catheter, and arterial blood Po2 by an indwelling electrode. PaOO2 remained near normal until just before pulmonary edema was grossly apparent, when it fell precipitously; left atrial pressure mounted to a peak and then declined. The apparent “steady-state” DlCO was reduced as much as 61%, but the dominant cause of hypoxemia was an increased venous admixture (shunt flow) on O2 breathing. Since the shunt was reversible by forcible inflation of the lungs, induced pulmonary edema was probably associated with closure of alveolar units. pulmonary venous admixture (shunt flow) and diffusing capacity; alveolar closure; arterial blood oxygen; tension in vivo; hypoxemia Submitted on August 14, 1963
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