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Unilateral smoke inhalation increases pulmonary blood flow to the injured lung.

Smoke inhalation (SI) affects the homogeneity of lung perfusion possibly by increasing alveolar surface tension. Anesthetized dogs (n = 8) were ventilated with a tracheal divider and a dual ventilator. One lung (left or right) was exposed to 5 minutes of SI while the other remained on room air. Total pulmonary blood flow (cardiac output) was measured by thermal dilution and left lung blood flow was measured with an ultrasonic flow probe. Since SI is associated with elevation of alveolar surface tension (AST), we studied a second group of dogs (n = 6) in which AST was increased in one lung with aerosolized dioctyl sodium sulfosuccinate (OT). The OT elevates AST without otherwise damaging the lung. Unilateral SI resulted in systemic hypoxemia (Pao2 fell from 91 +/- 6 to 55 +/- 4 mm Hg) and increased venous admixture (9 +/- 2% to 29 +/- 4%) both of which remained different from baseline values (p < 0.05) for 2 hours. Blood flow to the smoke exposed lung increased gradually and became significantly larger than that to the contralateral normal lung 2 hours following inhalation (smoke lung = 64% +/- 6% and normal lung = 36% +/- 6% of total blood flow). Following smoke exposure, pulmonary vascular resistance (PVR) increased with time in the unexposed normal lung (baseline = 8.7 +/- 1.4; 2 hours post smoke = 22.6 +/- 7.9 mm Hg/L/min, p < 0.05); PVR did not change in the smoke injured lung.(ABSTRACT TRUNCATED AT 250 WORDS)