Experimental study of the changes of α_1-adrenergic receptor in lung tissues after smoke inhalation injury in rats and the protective effects of prazosin on pulmonary smoke inhalation injury

Objective To investigate the changes of α 1-adrenergic receptor(α 1-AR) in lung tissues after smoke inhalation injury and the protective effects of prazosin on pulmonary smoke inhalation injury in rats. Methods The smoke inhalation injury model in rats was prepared with routine method, the lung water content and the pulmonary microvascular permeability (PMVP) were determined by use of the wet-dry weight ratio and Evans blue method respectively. The α 1-AR in rat's lung tissues was measured with radioreceptor analysis. Results The PMVP was evidently enlarged at 2th hour, peaked at 6th hour and still larger than that of normal control rats at 24th hour after smoke inhalation injury. The lung water content was increased significantly at 2 and 4th hour, and peaked at 24th hour. At 2,4,6 and 24th hour, the density of α 1-AR was elevated significantly, but the affinity of α 1-AR in rat's lung tissues was elevated only at 2th hour after smoke inhalation injury. There was a significant positive correlation between the increase of the density of α 1-AR and the enlargement of PMVP. In addition, prazosin 0.5, 1.5, and 3.0 mg/kg ip reduced the PMVP and the lung water content obviously, and attenuated the lung demage. Conclusion The mechanisms of pulmonary smoke inhalation injury in rats are related to the elevation of the density of α 1-AR in lung tissues, and prazosin has some protective effects on pulmonary smoke inhalation injury.