摘要
Objective To investigate the protective effects of hypertonic-hyperoncotic solution(HHS) on the acute lung injury induced by lipopolysacchharide in rats.Methods Models of acute lung injury(ALI) in rats were induced by lipopolysacchharide(LPS,5 mg/kg,i.v.). Twenty-four SD rats weighing 180 g-200 g were randomly divided into 3 groups with 8 animals each: ① control group received only normal saline;② LPS group received intravenous LPS 5 mg/kg;③ HHS group received HHS 4 ml/kg infusion 2 min after intravenous LPS 5 mg/kg.The rats were anesthetized with urethane.They were killed by exsanguinations at 4 h after intravenous LPS or normal saline administration.Then the lungs were removed,left lung was lavaged and the bronchoalveolar lavage fluid(BALF) was collected for determination of albumin concentration.Right lung was used for measurement of wet/dry lung weight ratio and myeloperoxiase(MPO) activity.Pathologic changes of lung tissue were observed microscopically.Results Obvious ALI pathological manifestation in the lungs of LPS group rats was observed compared with NS group,and wet/dry lung weight ratio and MPO activity in lungs increased significantly in LPS group(P<0.01) as well as the albumin concentration in BALF(P<0.01).Compared with LPS group,the pathological manifestation in the lungs was ameliorated and wet/dry lung weight ratio,MPO activity in lungs and the albumin concentration in BALF decreased significantly in HHS group(P<0.01).Conclusion HHS can attenuates lipopolysacchharide-induced ALI in rats probably through inhibition of the infiltration and activation of neutrophil.
Objective To investigate the protective effects of hypertonic-hyperoncotic solution （HHS） on the acute lung injury induced by lipopolysacchharide in rats. Methods Models of acute lung injury （ALI） in rats were induced by lipopolysacchharide （LPS, 5 mg/kg, i. v. ）, Twenty-four SD rats weighing 180 g - 200 g were randomly divided into 3 groups with 8 animals each： ① control group received only normal saline;② LPS group received intravenous LPS 5 mg/kg; ③ HHS group received HHS 4 ml/kg infusion 2 min after intravenous LPS 5 mg/kg. Tne rats were anesthetized with methane. Tney were killed by exsanguinations at 4 h after intravenous LPS or normal saline administration. Then the lungs were removed, left lung was lavaged and the bronchoalveolar lavage fluid （BALF） was collected for determination of albumin concentration. Right lung was used for measurement of wet/dry lung weight ratio and myeloperoxiase （MPO） activity. Pathologic changes of lung tissue were observed microscopically. Results Obvious ALI pathological manifestation in the lungs of LPS group rats was observed compared with NS group, and wet/dry lung weight ratio and MPO activity in lungs increased significantly in LPS group（P 〈0.01 ） as well as the albumin concentration in BALF（P 〈0.01 ）. Compared with LPS group, the pathological manifestation in the lungs was ameliorated and wet/dry lung weight ratio, MPO activity in lungs and the albumin concentration in BALF decreased significantly in HHS group （P 〈0. 01 ）. Conclusion HHS can attenuates lipopolysacchharide-induced ALI in rats probably through inhibition of the infiltration and activation of neutrophil.
出处
《国际麻醉学与复苏杂志》
CAS
2006年第2期79-81,共3页
International Journal of Anesthesiology and Resuscitation
