Abstract： Objective To explore changes in the distribution of pulmonary surfactant (PS)subtypes in alveolar spaces and the possible mechanisms involved, and also to investigate the relationship between changes and the inhibition of PS activity after smoke inhalation. Methods Following induction of smoke inhalation injury in rats, arterial blood gas levels, lung water volume, surface tension of bronchoalveolar lavage fluid ( BALF), contents of total phospholipids ( TPL), total proteins ( TP), albumin ( alb), and activity of α1-antitrypsin (α1-AT) in BALF, the uhrastructures of PS subtypes in alveolar spaces were determined respectively in normal control and injured animals at 2 h, 6 h, 12 h and 24 h after injury. Results After smoke inhalation, the animals displayed acute respiratory failure and serious pulmonary edema, progressive elevation of minimum surface tension (Stmin) in BALF, marked increase in the levels of TPL, TP, Alb, and α1-AT in BALF., and significant correlation between changes in Stmin and α1-AT/TP ratio, as well as in α1-AT/Alb ratio. In the early stage after injury, lamellar bodies and vesicles aggregated in alveolar spaces with destruction of tubular myelins, while a great many vesicles and a few lamellar bodies aggregated, with obvious deficiency in tubular myelins in the late stage. Conclusions Changes in the distribution and abnormal conversion of PS subtypes in alveolar spaces are one of the important causes for the inhibition of PS activity after smoke inhalation, and the imbalance of α1-AT/plasma proteins ratio may play an important role in it.