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作 者:宋志芳[1] 谢伟[1] 单慧敏[1] 郭晓红[1] 孙波[2]
机构地区:[1]上海第二医科大学新华医院成人ICU,200092 [2]上海复旦大学儿科医院小儿呼吸急救实验室,200005
出 处:《中国危重病急救医学》2006年第12期716-720,共5页Chinese Critical Care Medicine
基 金:上海市卫生局科技发展基金资助项目(00409)
摘 要:目的研究糖皮质激素(GC)治疗感染性急性呼吸窘迫综合征(ARDS)的临床价值。方法大肠杆菌腹腔注射制备猪ARDS模型。健康雄性幼猪9头,按随机原则分为对照组(n=3)、早期治疗组(n=4)和中期治疗组(n=2);甲基泼尼松龙20mg(4mg·kg-1·d-1)静脉注射,12h1次;观察动物各项生理指标与生存时间;72h处死动物,常规方法检测肺组织湿/干重(W/D)比值,光镜下Smith评分法观察病理学改变。结果早、中期治疗组动物存活时间长于对照组,但差异均无显著性(P均>0.05);早期治疗组氧合指数(PaO2/FiO2)和平均动脉压(MAP)均较对照组改善明显(P均<0.05),中期治疗组自身对照PaO2/FiO2和MAP也明显改善(P<0.05或P<0.01);除早期治疗组总蛋白(TP)显著高于中期治疗组外,各组支气管肺泡灌洗液(BALF)中总磷脂(TPL)、饱和磷脂酰胆碱(DSPC)、白细胞计数以及肺表面张力、肺W/D比值差异均无显著性(P均>0.05);早、中期治疗组肺组织病理学改变较对照组均加重(P均<0.01)。结论GC能改善感染性ARDS低氧血症与休克,对终末期肺表面活性物质、表面张力和形态学改变无明显影响。Objective To evaluate the effect of glucocorticoid (GC) in the treatment of septic acute respiratory distress syndrome (ARDS). Methods ARDS model was reproduced by intraperitoneal injection of E. coli in piglets. Nine male piglets were randomly divided into control (C group), early (GC1) and middle (GC2) stage treatment groups. In the latter two groups methylprednisolone 20 mg was intravenously, given every 12 hours (4 mg^-1 · kg^-1 · d^-1). All of the clinical data and survival time during 72 hours were collected and analyzed, including the collection of bronchialalveolar lavage fluid (BALF) for the determination of total protein (TP), total phospholipids (TPL), disaturated phosphatidyl choline (DSPC), and measurement of alveolar tension. Ratio of pulmonary wet and dry (W/D) weight was determined routinely, and pathological changes and their severity were evaluated by optical microscope and Smith scores. Results ARDS model was reproduced at (8.3 ± 8.5) hours, and survival time of three groups was (11.0±6.6) hours, (35.3±12.5) hours and (52.5± 13.8) hours respectively. Animals in GC1 and GC2 survived longer than those in C group, but there was no statistically significant difference among them (both P^0.05). Oxygen index (PaOz/FiOz) and mean arterial pressure (MAP) were improved in GC1 much better than those of controls (both P〈0.05), and the same was true in GC2 as compared that before GC treatment (P〈0.05 or P〈0.01). There were no significant differences among TPL, DSPC, white blood cell count (WBC) of BALF in each group, so were lung surface tension and W/D (all P〉0.05). TP of BALF was significantly higher in GC1 than that in GC2. Compared with C group, alveolar and interstitial edema, inflammation and hemorrhage were more severe in GC1 (all P 〈 0.01 ), hyaline membrane was less (P〈0.01) and no difference in atelectasis (P〉0.05). The alveolar and interstitial edema and inflammation in GC2 wer
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