血必净联合乌司他丁对脓毒症休克患者心肌损伤的保护作用

The Protective Effect of XUEBIJING Injection and Ulinastatin on the Myocardial Damage in the Patients with Septic Shock

目的:探讨血必净与乌司他丁对脓毒性休克患者心肌损伤的保护作用。方法:66例伴有心肌损伤的脓毒症休克患者随机分为对照组(A组,n=22例)、血必净组(B组,n=22)和联合治疗组(C组,n=22)。A组按2008国际严重脓毒症和脓毒症休克治疗指南给予抗感染、液体复苏及营养支持等经典治疗,B组在经典治疗基础上加用血必净注射液(50 ml,1次/12小时,连用7天),C组在B组基础上联合乌司他丁治疗(20w U,静脉泵入,1次/8小时,连续7天)。观察3组患者治疗前后急性生理学与既往健康状况Ⅱ(APACHEⅡ)评分、肌钙蛋白Ⅰ(c Tn I)、肿瘤坏死因子(TNF-a)、白细胞介素6(IL-6)、脑钠肽(BNP)、肌酸激酶同工酶(CK-MB)、乳酸脱氢酶(LDH)变化。结果 :3组患者治疗前各项指标均无显著差异(P>0.05);治疗7天后,C组的APACHEⅡ、c Tn-Ⅰ、BNP、CK-MB、LDH、TNF-a、IL-6水平较A组(P<0.01)和B组(P<0.01)均显著下降。结论 :血必净联合乌司他丁可能通过降低体内的炎症级联反应来减轻脓毒症休克患者的心肌损伤。

Objective ：To discuss the protective effect of XUEBIJING injection and Ulinastatin on the myocardial damage in the patients with septic shock. Methods ：66 cases of patients with myocardial damage and septic shock were included and randomly divided into control group（group A, n =22）, Xuebijing Treatment group（group B, n =22） and Combining treatment group（group C,n =22）. Patients in the group A were given conventional treatments according to the septic diagnostic and treatment guidelines made by SSC in 2008, like anti-infection, fluid ？resuscitation and nutrition. Patients in the group B were received conventional treatments plus Xuebijing injection（50ml,1 / 12 h through intravenous drop for consecutive 7 days）, patients in the group C was given combining treatment of Xuebijing injection and Ulinastatin（20 w U, 1 / 8h through intravenous injection pump for consecutive 7 days）. The APACHE Ⅱ scores, the level of cTnI, TNF-α,IL-6,BNP,CK-MB and LDH were recorded before and after the treatment. Results ： There were no significant differences in the APACHE Ⅱ scores, the level of cTnI, TNF-α,IL-6,BNP,CK-MB and LDH before treatment between two groups（P 〉0.05）. After 7 days of treatment, the above parameters were all significantly decreased in the group C compared with those in group A（P 〈0.01）and group B（P 〈0.01）. Conclusion ： Combining treatment of Xuebijing injection and ulinastatin can relieve the sepsis-induced myocardial damage in patients with septic shock through the mechanism of reducing the inflammatory cascade reaction.