Smoke inhalation can produce acute pulmonary edema. Previous studies have shown that the bronchial arteries are important in acute pulmonary edema occurring after inhalation of a synthetic smoke containing acrolein, a common smoke toxin. We hypothesized that inhalation of smoke from burning cotton, known to contain acrolein, would produce in sheep acute pulmonary edema that was mediated by the bronchial circulation. We reasoned that occluding the bronchial arteries would eliminate smoke-induced pulmonary edema, whereas occlusion of the pulmonary artery would not. Smoke inhalation increased lung lymph flow from baseline from 2.4 ± 0.7 to 5.6 ± 1.2 ml/0.5 h at 30 min ( P < 0.05) to 9.1 ± 1 ml/0.5 h at 4 h ( P < 0.05). Bronchial artery ligation diminished and delayed the rise in lymph flow with baseline at 2.8 ± 0.7 ml/0.5 h rising to 3.1 ± 0.8 ml/0.5 h at 30 min to 6.5 ± 1.5 ml/0.5 h at 240 min ( P < 0.05). Wet-to-dry ratio was 4.1 ± 0.2 in control, 5.1 ± 0.3 in smoke inhalation ( P< 0.05), and 4.4 ± 0.4 in bronchial artery ligation plus smoke-inhalation group. Smoke inhalation after occlusion of the right pulmonary artery resulted in a wet-to-dry ratio after 4 h in the right lung of 5.5 ± 0.8 ( P < 0.05 vs. control) and in the left nonoccluded lung of 5.01 ± 0.7 ( P < 0.05). Thus the bronchial arteries may be major contributors to acute pulmonary and airway edema following smoke inhalation because the edema occurs in the lung with the pulmonary artery occluded but not in the lungs with bronchial arteries ligated.
Genetics of pulmonary hypertension and high-altitude pulmonary edema
