盐酸戊乙奎醚对胃蛋白酶误吸大鼠模型肺的保护作用

Study on the Pulmonary Protective Effect of Penehyclidine Hydrochloric in Rats' Pepsin Aspiration

目的观察盐酸戊乙奎醚对胃蛋白酶误吸所致急性肺损伤大鼠模型肺炎性因子的变化。方法采用气管内注入胃蛋白酶法制作大鼠肺误吸模型。将健康雄性Wistar大鼠45只随机分为3组:空白对照组(C组);生理盐水对照组(NSC组);盐酸戊乙奎醚组(PHI组)。观察胃蛋白酶注入气管后大鼠平均动脉压(MAP)和心率(HR),用ELISA法测肺泡灌洗液上清和血清中的TNF-α和IL-66的量。光镜观察肺组织病理变化。结果胃蛋白酶法大鼠肺误吸模型建立成功。NSC组HR,MAP先升高后降低;C组HR,MAP较平稳,与NSC组比较,差异均有统计学意义(P<0.01);PHI组经治疗后两者均趋于平稳,与NSC比较差异有统计学意义(P<0.01)。除C组外各组大鼠肺泡灌洗液上清和血清中的TNF-α和IL-66两者含量均升高(P<0.01);与NSC组比较,PHI组TNF-α和IL-6含量降低(P<0.05)。病理学结果显示:肺组织损伤程度PHI组较NSC组明显减轻。结论盐酸戊乙奎醚可以减轻肺误吸所致急性肺损伤的炎症反应,对胃蛋白酶误吸大鼠肺有保护作用。

Objective To investigate the influence of penehyelidine hydrochloride on pneumonia factor in rats being acute lung injury（AI,I） due to Pepsin. Methods Animal models were made in method of instilling pepsin in rats intratracheally. Forty-five Ileahhy male wistar rats were raudnmly divided into 3 groups ： control group （ group C） ; normal saline group （ group NSC ） ; penehyclidine hydnachloride group （（;roup PHI）. Mean arterial pressure{ MAP） and heart rate（ HR） were observed after pepsin injected into the trachea. The amount of TNF- αin and IL-6 in serum and suiw, rnataut of lavaging fluid from bronchoalveolar was measured with ELISA. The pulmonary tissue pattlological change was investigated by light microscopy. Results Rats＇pulmonary pepsin-aspirated model was established successfully. HR and MAP in grmtp NSC elevated then reduced, and group C kept stable relatively, so the differences between them were significant statistically （P 〈 0. Ol ） ; HR and MAP both stabilized after treatment in group PHI,so differences between group PHI and NSC was significant statistically （ P 〈 0. Ol ）. Amounts of TNF-αin supernatant and IL-6 in serum increased in all groups except for group C（P 〈 0. O1 ）. TNF-α and IL-6 decreased in group PHI compared with group NSC（ P 〈 0.05 ）. Pathological results showed ：pulmonary tissue injury relieved better in group PHI than NSC obviously. Conclusion These resuhs suggest that penehyclidine hydroehloride can reduce the inflammatory response to ALl and prevent from respiratory failure induced by pepsin aspiration.