翁翠莲++刘庆华

[摘要] 目的 探討地塞米松对内毒素（ET）致急性肺损伤（ALI）兔心肌保护作用的机理。 方法 日本大白兔24只随机分为生理盐水对照组（A组）、ET组（B组）和ET致伤+地塞米松干预组（C组），每组8只。除了A组以外，B组、C组均从颈静脉给予ET（700 μg/kg），C组在给予ET前予地塞米松5 mg/kg。分别于0 h、0.5 h、1 h、2 h、4 h观察动脉血气变化。4 h后处死动物，取肺、心脏组织观察光镜下的组织病理学改变，并检测心脏中心肌型脂肪酸结合蛋白（H-FABP）的变化。 结果 B组动物血氧饱和度在0.5 h明显下降（265.4±70.2）mmHg，肺组织明显渗出，水肿液形成，透明膜形成，肺间质血管内皮细胞肿胀，血管壁见较多的中性粒细胞贴壁。心肌组织细胞肿胀，心肌结构排列紊乱，局灶可见心肌细胞坏死。与A组比较，B组心组织中的H- FABP明显降低[（302.0±89.1） vs （132.6±46.9），P<0.01]。与B组比较，C组的动脉血氧饱和度显著升高，心肌中的H-FABP明显高于ET组，差异有统计学意义[分别为（236.0±88.1） vs （132.6±46.9），P<0.05]，心肌损伤较损伤组明显轻。 结论 ET所致ALI的心肌损伤作用可能与H-FABP的减少有关，使用地塞米松能增加H-FABP的含量，减轻肺损伤时的心肌受损作用。

[关键词] 急性肺损伤；心脏型脂肪酸结合蛋白；地塞米松

[中图分类号] R563 [文献标识码] A [文章编号] 1673-9701（2017）26-0034-04

Effects of dexamethasone on myocardial injury in rabbits with acute lung injury

WENG Cuilian1，2 LIU Qinghua3

1.Department of Respiratory Medicine， Fujian Provincial Hospital， Fuzhou 350000， China； 2.Department of Respiratory Medicine， the First Hospital of Xiamen University， Xiamen 361000， China； 3.E.N.T. Department， Fujian Provincial Hospital， Fuzhou 350000， China

[Abstract] Objective To investigate the mechanism of protective effect of dexamethasone on myocardium in the rabbits with endotoxin （ET） induced acute lung injury （ALI）. Methods 24 Japanese rabbits were randomly divided into normal saline control group （group A）， ET group （group B） and ET-induced injury+dexamethasone intervention group （group C）， with 8 rabbits in each group. In addition to group A， group B and group C were given ET（700 μg/kg） via the jugular vein. Group C was given dexamethasone 5 mg/kg before administration of ET. The changes of arterial blood gas were observed at 0 h， 0.5 h， 1 h， 2 h and 4 h respectively. After 4 h， animals were sacrificed， lung and heart tissues were harvested and histopathological changes were observed under light microscope. Changes in the H-FABP were detected in heart. Results The animal oxygen saturation in group B was significantly decreased at 0.5 h（265.4±70.2 mmHg）. Lung tissue was oozing significantly. Edema fluid was formed， and transparent membrane was formed. Pulmonary interstitial vascular endothelial cells were swelling. There were more neutrophils adhering to the wall in vascular wall. Myocardial tissue cells were swelling， and myocardial structure was in disorder. Myocardial cell necrosis could be seen in local focus. Compared with group A， H-FABP in group B was significantly lower than that in group A （302.0±89.1） vs （132.6±46.9，P<0.01）. Compared with group B， the arterial oxygen saturation in group C was significantly higher. The H-FABP in the myocardium was significantly higher than that in the ET group， and the difference was statistically significant [（236.0±88.1） vs （132.6±46.9， P<0.05）]. Myocardial injury was significantly milder than that in the injury group. Conclusion The myocardial injury induced by ET may be related to the decrease of H-FABP. The application of dexamethasone can increase the content of H-FABP and reduce the myocardial damage during lung injury.endprint

[Key words] Acute lung injury （ALI）； H-FABP； Dexamethasone

急性呼吸窘迫綜合征（ARDS）是一个危重病综合征，其特点是急性呼吸窘迫和严重的低氧血症，每年大于100万的人患有ARDS[1]。严重的感染、败血症、严重创伤或烧伤、急性胰腺炎导致肺的直接损伤。在所有原因中，革兰阴性细菌感染造成的败血症是最常见的病因，大约有25%的ARDs是由严重败血症所致[2，3]。内毒素（ET）是革兰阴性细菌细胞壁的脂多糖成分，能引起ARDS，并演变为多脏器功能衰竭如心衰、肾衰等。心肌型脂肪酸结合蛋白（H-FABP）在心肌细胞中高表达，研究表明其可以作为心肌损伤早期敏感的指标。本实验使用内毒素肺损伤（ALI）模型来监测心肌组织中H-FABP含量的变化，探讨ALI时心脏损伤的机制和地塞米松对其保护性作用。……