肿瘤坏死因子-α、内毒素、白细胞介素-6、磷脂酶A2与重症胸腹损伤后急性心肌细胞损伤的相关性

目的探讨肿瘤坏死因子-α（TNF-α）、内毒素（LPS）、白细胞介素-6（IL-6）、磷脂酶A1（PLA2）与重症胸腹损伤后心肌细胞损伤发生的关系。方法收集2009年1月-2013年6月在我院急诊科就诊，创伤指数（TI）≥17分，除外合并颅脑损伤及在急诊死亡的胸腹损伤患者112例，在救治的同时检查肌酸激酶同工酶（CK-MB）、心肌肌钙蛋白T（cTnT）、TNF-α、LPS、IL-6、PLA2，对检验结果进行相关性分析。结果心肌损伤：CK-MB：（218．79±21．59）U／L，cTnT：（546．254±29．34）ng／L；损伤因子：TNF-α（39．614±13．09）μg／L，LPS：（453．684±96．37）IU／L，IL-6：（436．83±113．86）μg／L，PLA2：（48．354±12．26）μg／L。CK-MB与TNF-α、LPS、IL-6、PLA2比较相关系数（r）均〉0．8832，cTnT与TNF-α、LPS、IL-6、PLA2比较r均〉0．889l，均呈显著正相关。结论TNF-α、LPS、IL-6、PLA2参与了重症胸腹损伤后心肌细胞损伤的发生，对TNF-α、LPS、IL-6、PLA2的针对性干预，或有可能减轻重症胸腹损伤后心肌细胞损伤的程度，提高重症胸腹损伤者的生存率。

Correlation between tumor necrosis factor-s,lipopolysaccharide, interleukin-6 and phospholipase A2 and acute myocardial cell disorders after severe thoracico-abdominal injury

Objective To investigate the correlation between tumor necrosis factor-α （TNF-α） , lipopolysaccharide （LPS） , inter- leukin-6 （1L-6） and phosphollpase A2 （PLA2） and myocardial cell disorders in severe thoraeieo-abdominal injury. Methods A total of 112 patients with severe thoraeieo-abdominal injury, admitted to PLA No. 253 Hospital from January 2009 to June 2013, were enrolled in the study. All the patients＇ trauma index （TI） was above or equal to 17. As the rescue and treatment were in pro- gress, they were examined ereatine kinas-MB （CK-MB） , cardiac troponin T （cTnT） , TNF-α, LPS, IL-6 and PLA2 for analysis on correlation. Results The myocardial cell injury test results were as follows ： CK-MB （ 218.79 ＋ 21.59 ） U/L, eTnT ： （ 546.25 ± 29.34） ng/L. The injury factor test results were as follows ： TNF-α （ 39.6t ± 13.09 ） μg/L, LPS （453.68 ± 96.37 ） IU/L, IL-6 （ 436.83 ± 113.86 ） μg/I,, PLA2 （48.35± 12.26） μg/L. Both the CK-MB and cTnT were obviously correlative with TNF-α, LPS, IL-6 and PLA2 （ r 〉 0. 883 2, r 〉 0. 889 1 ）. Conclusion TNF-α, LPS, IL-6 and PLA2 all participate in the process of the acute myocardial cell disorders in severe thoracico-abdominal injury. The prophase interference in TNF-α, LPS, IL-6 and PLA2 may help to improve the myocardial cell dysfunction in severe thoracieo-abdominal injury.