内毒素、磷脂酶A2与颅脑损伤后心肌功能损害的相关性与机制探讨

目的探讨内毒素（LPS）、磷脂酶A2（PLA2）与重型颅脑损伤后心肌功能损害发生的相关性及机制。方法收集2009年1月-2011年12月在中国人民解放军第二五三医院急诊科就诊的创伤指数TI≥17分、格拉斯哥昏迷评分GCS≤12分，并除外合并其他部位损伤及在急诊科内死亡的急性重型颅脑损伤患者53例，在急诊予以相应抢救、治疗的同时抽血检查肌酸激酶同工酶（CK-MB）、心肌肌钙蛋白T（cTnT）、LPS、PLA，，对检验结果进行相关性分析检验。以同期到笔者医院门诊体检的健康志愿者为对照组，共计53例，在门诊体检中心抽血行相同检查，试验组与对照组检测数据比较用t检验。结果心肌功能检验结果：试验组：CK-MB：73．52±26．41U／L，eTnT：184．83±68．98pg／ml；对照组：CK-MB：8．13±3．64U／L，cTnT：21．67±11．58pg/ml。损伤因子检验结果：试验组：LPS：309．38±49．41IU／L，PLA，：45．23±19．97ng／ml；对照组：LPS：87．38±46．51IU／L，PLA，：7．47±5．21ng／ml。试验组与对照组有显著差异。反映心肌功能的指标CK-MB和eTnT与可能导致心肌细胞损害的因素LPS、PLA2之间存在着显著的相关性。结论LPS、PLA2可能通过颅脑损伤后的应激反应、微循环障碍、炎症反应的“瀑布样”效应、肠源性内毒素血症等途径参与了颅脑损伤后心肌细胞功能损害的发生、发展。因此在颅脑损伤后的早期加强对心肌细胞的功能保护，加强对LPS、PLA：的针对性干预，抑制LPS、PLA2的高表达，有可能减少颅脑损伤后心肌细胞功能损害的发生。

Study of the Relationship between Myocardial Damage and LPS,PLAz in Traumatic Brain Injury.

Objective To study the function and possible mechanism of lipopolysaccharide （LPS） , phospholipase A2 （PLA2） in myocardial damage after acute severe brain injury. Methods Fifty three cases of patients with acute severe brain injury from January 2009 to December 2011 in emergency department of 253 hospital of PLA were included in this study, with their trauma index （TI） 〉t 17, Glasgow coma score （GCS） score≤ 12, except the patients with the other parts of injury and died in emergency department. All patients were given corresponding treatment in the emergency. We examined their blood of creatine kinase isoenzyme （ CK - MB） , cardiac troponin T （cTnT） ,LPS, PLA2 , analyzed the relationship of test result. 53 cases of health volunteers served as control group. Results Myocardial function test results ： In test group, CK - MB was 73.52 ±26.41 U/L, cTnT 184.83 ± 68.98pg/ml ; in control group, CK - MB was 8.13 ± 3.64U/L, cTnT 21.67 ~ 11.58pg/ml. Damage factor test results：in test group, LPS was 309.38 ± 49.41IU/L, PLA2 45.23 ± 19.97ng/ml; in control group, LPS was 87.38 ± 46.51IU/L, PLA2：7.47 ± 5.21ng/ml. There was significant difference and significant relationship be- tween them. Conclusion LPS and PLA2 may be involved in the occurrence, development of myocardial damage after severe brain injury. Strong stress response, microcirculation disturbance, inflammation, intestinal endotoxemia after severe traumatic brain injury is possible mechanism. So the protective effect on myocardial function and intervention effect to LPS and PLA2 in the early stage may reduce the myo- cardial function damage after severe brain injury.