灯盏花素对感染性休克患者心肌损伤的保护作用

Protective effect of breviscapine on myocardial damage of patients with septic shock

目的 探讨灯盏花素对感染性休克患者心肌损伤的保护作用及其可能作用机制。方法 将60例感染性休克合并心肌损伤患者随机分为对照组和灯盏花素组，每组30例，均按照感染性休克指南行集束化治疗，灯盏花素组在常规治疗基础上加用灯盏花素注射液20 mg，溶于5%葡萄糖注射液250 mL中，每天1次，静脉滴注，10 d为一个疗程。分别于治疗前和治疗7、10 d后采集空腹静脉血，测定血清心肌肌钙蛋白I（cardiac troponin I，cTnI）、B-型脑钠肽（B-type natriuretic peptide，BNP）、肿瘤坏死因子-α（tumor necrosis factor-α，TNF-α）及超氧化物歧化酶（superoxide dismutase, SOD）的水平，并观察两组不良反应发生情况。结果 与治疗前比较，两组患者治疗7、10 d后血清cTnI、BNP及TNF-α水平均明显下降（P〈0.05），SOD活性均明显升高（P〈0.05）。与对照组比较，灯盏花素组治疗7、10 d后血清cTnI、BNP及TNF-α水平明显下降（P〈0.05），SOD活性明显升高（P〈0.05）。两组患者治疗过程中均无严重不良反应发生。结论 灯盏花素可以明显减轻感染性休克患者的心肌损伤程度，推测其机制可能与其抑制炎性反应、抗氧化应激作用有关。

Objective To explore the myocardial protective effect of breviscapine and its possible mechanism in patients with septic shock. Methods Sixty patients with septic shock complicating with myocardial injury were randomly divided into two groups （ n = 30, each） ： control group and breviscapine group. Every patient received sepsis bundle therapy according to the International Sepsis Guidelines, breviscapine group was treated with additional breviscapine （20 mg＋ 5% GS 250 mL, iv, qd × 10 d）. Blood samples were taken from fasting vein at various time points ： before treatment, 7 and 10 d after treatment for determination of plasma concentration of cardiac troponin I （cTnI）, brain natriuretic peptide （ BNP）, tumor necrosis factor - α （ TNF -α） and superoxide dismutase （ SOD）, and the adverse events were observed. Results Compared with before treatment, the levels of cTnI, BNP, and TNF-α in each group were significantly decreased at 7, 10 d after treatment, while the SOD activity was significantly increased at 7, 10 d after treatment （P 〈 0.05）. Compared with control group, the levels of cTnI, BNP, and TNF - α were significantly decreased. While the SOD activity was significantly increased at 7, 10 d after treatment in breviscapine group （ P 〈 0.05 ）. There were no severe adverse events in each group during the treatment. Conclusion Breviscapine can significantly decrease the severity of myocardial injury in patients with septic shock, and the mechanism may be related to the anti - inflammatory and anti - oxidative stress effect.