海水和脂多糖吸入肺损伤的比较研究  

Comparison of lung injuries induced by seawater and lipopolysaccharide inhalation

作　　者：邓朝霞[1] 王关嵩[1] 钱桂生[1] 杨昱[1] 周长喜[1] 

机构地区：[1]第三军医大学新桥医院全军呼吸内科研究所,重庆400037

出　　处：《解放军医学杂志》2009年第4期381-384,共4页Medical Journal of Chinese People's Liberation Army

基　　金：国家自然科学基金资助项目(30770928);军队"十一五"攻关课题(06G083);重庆市自然科学基金资助项目(2007BB5072);第三军医大学科研基金资助项目(2006HG04)

摘　　要：目的比较海水型急性肺损伤(SW-ALI)和脂多糖(LPS)型急性肺损伤(LPS-ALI)的特点,为SW-ALI的治疗提供依据。方法将48只Wistar大鼠随机均分为对照组、海水组、LPS组,每组16只,海水组和LPS组分别吸入海水(4ml/kg)和LPS(4mg/kg)建立ALI模型,分别于建模前及建模后0.5、1、2、4、8h进行动脉血气分析,并于8h后检测肺微血管通透性(PMVP)、血管外肺水含量指数(EVLWI)、肺组织髓过氧化物酶(MPO)及丙二醛(MDA)含量、Na+-K+-ATP酶(NKA)活性,并观察肺组织病理学变化。结果海水组和LPS组在吸入海水和LPS后,动脉血氧分压(PaO2)迅速下降,30min时最低,分别为40.62±5.04、41.35±5.77mmHg,8h后虽然逐渐回升至52.83±6.38、58.35±7.01mmHg,但仍显著低于对照组(99.67±6.95mmHg,P<0.01);吸入海水和LPS后,PMVP分别增高至98.57±16.63、82.32±13.84μg/g,EVLWI分别增高至0.68±0.09、0.52±0.05,MPO分别增高至4.05±0.35、3.97±0.41U/g,MDA分别增高至5.73±0.48、5.95±0.51nmol/mg,NKA活性则分别降至3.35±0.26、3.18±0.22μmol/(mg.h)。在2h时点以后,海水组的PaO2显著低于LPS组(P<0.05),PMVP、EVLWI显著高于LPS组(P<0.05),而两组的MDA、MPO含量和NKA活性无显著性差异。海水组肺水肿、肺泡内出血、炎性细胞浸润较LPS组重。结论与LPS-ALI比较,海水吸入所致的ALI引起的肺水肿更加严重。Objective To compare the features of seawater-induced acute lung injury （SW ALl） with the lipopolysaccharide （LPS） induced lung injury （LPS -ALI） to look for a treatment modality of SW-ALI. Methods Forty-eight Wistar rats were randomly divided into 3 groups： control group, seawater inhalation group （SWI） and lipopolysaccharide inhalation group （LPSI）. Acute lung injury （ALI） rat models were reproduced either by seawater （4ml/kg） or LPS （4mg/kg） inhalation in SWI group and LPSI group, respectively. PaO2, PaCQ, and pH were determined at baseline and at 30min, lh, 2h, 4h and 8h after the establishment of ALI models. Pulmonary microvascular permeability （PMVP）, extravascular lung water index （EVLWI）, myeloperoxidase （MPO）, malondialdehyde （MDA） and Na^-K- ATP activity （NKA） in lung homogenate were measured by biochemical methods, and pathological changes were also examined under microscope. Results PaO2 declined rapidly after seawater or LPS inhalation. At 30min time point, the PaO2 was down to 40. 62±5. 04mmHg in SWI group, which was the lowest value, and to 41.35±5. 77mmHg in LPSI group. Although the PaO, went up to 52. 83 ±6. 38 and 58. 35±7. 01mmHg, respectively, at 8h time point in both groups, it was still lower than that in control group （99. 67±6.95mmHg, P〈0. 01）. After seawater or LPS inhalation, PMVP increased to 98. 57±16. 63μg/g and 82. 32±13. 84μg/g, EVLWI in- creased to 0. 68±0. 09 and 0. 52±0. 05, MPO increased to 4. 05±0. 35U/g and 3. 97±0.41U/g, MDA increased to 5. 73±0. 48nmol/mg and 5. 95±0. 51nmol/mg, while ,NVKA decreased to 3. 35±0. 26μmol/（mg·h） and 3. 18±0. 22gmol/（mg·h）, respectively, in SWI group and LPSI group. Two hours after model establishment, PaO2 in SWI group was markedly lower, while the PMVP and EVLWI were significantly higher than that in LPSI group （P〈0. 05）. No significant difference was found in MPO, MDA and NKA between both groups, but pulmonary edema, alveoli hemorrhage and inflammato

关 键 词：海水 呼吸窘迫综合征 成人 脂多糖类 肺水肿 

分 类 号：R563.9[医药卫生—呼吸系统]