天津医药

天津医药 ›› 2019, Vol. 47 ›› Issue (4): 387-390.doi: 10.11958/20190108

• 实验研究 • 上一篇    下一篇

ERK抑制剂对心肺复苏后大鼠心肌缺血再灌注损伤和能量代谢的作用研究

陶冉 1，谢露 2，郑君慧 1，谭小风 1，李诺 1，覃涛 1，杨叶桂 1，陈蒙华 1△   

  1. 1广西医科大学第二附属医院 ICU（邮编 530007）；2广西医科大学基础医学院生理学教研室
  • 收稿日期:2019-01-15 修回日期:2019-02-15 出版日期:2019-04-15 发布日期:2019-05-27
  • 通讯作者: 陶冉 E-mail:taoran4069@163.com
  • 作者简介:陶冉（1992），男，硕士在读，主要从事心血管重症及心肺脑复苏研究
  • 基金资助:
    ERK抑制剂逆调节心肺复苏后脑组织线粒体融合/分裂失衡，抑制神经 细胞凋亡机制研究;控制性高血钾改善心脏骤停/心肺复苏后全脑缺血再灌注损伤的作用及 其机制研究;ERK抑制剂经由线粒体动力学-自噬途径促进心肺复苏后神经细胞生存 研究

Effects of ERK inhibitor on myocardial ischemia reperfusion injury and energy metabolism dysfunction in rats after cardiopulmonary resuscitation

TAO Ran1, XIE Lu2, ZHENG Jun-hui1, TAN Xiao-feng1, LI Nuo1, QIN Tao1, YANG Ye-gui1, CHEN Meng-hua1△   

  1. 1 The Intensive Care Unit of the Second Affiliated Hospital of Guangxi Medical University, Nanning 530007, China; 2 Department of Physiology, Pre-Clinical Science, Guangxi Medical University
  • Received:2019-01-15 Revised:2019-02-15 Published:2019-04-15 Online:2019-05-27
  • Contact: Ran Tao E-mail:taoran4069@163.com

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摘要： 目的 探讨 ERK抑制剂 PD98059对于心脏骤停/心肺复苏（CA/CPR）后大鼠心肌能量代谢和心肌缺血再灌 注损伤的作用。方法 36只大鼠按随机数字表法分为假手术（Sham）组（n=6）、模型（CA）组（n=15）和 PD98059（PD） 组（n=15）。Sham组只单纯行手术操作；CA组和 PD组经食道交流电刺激诱导心室颤动（VF）建立大鼠 CA/CPR模型， 恢复自主循环（ROSC）后，PD组立即静脉注射 PD98059（0.3 mg/kg），CA组立即静脉注射等量生理盐水。观察复苏后 24 h存活情况，采集血清检测心肌肌钙蛋白 I，同时取心肌组织进行 HE染色、ATP含量测定，并采用蛋白免疫印迹法 检测磷酸化 ERK（p-ERK）的表达水平。结果 复苏后 24 h，各组存活情况为 Sham组 6只、CA组 6只、PD组 13只。与 Sham组比较，CA和 PD组血清心肌肌钙蛋白 I水平升高；PD组血清心肌肌钙蛋白 I水平较 CA组下降（P＜0.05）。PD 组 ATP含量较 CA组明显升高（P＜0.05），心肌病理损伤程度也较 CA组明显减轻。与 Sham组比较，CA和 PD组大鼠 心肌组织 p-ERK的表达水平升高；PD组 p-ERK表达水平较 CA组下降（P＜0.05）。结论 ERK抑制剂 PD98059治疗 能够改善心肺复苏后心肌能量代谢障碍，减轻心肌缺血再灌注损伤。

关键词: 心脏骤停, 心肺复苏, 缺血再灌注损伤, 能量代谢

Abstract: Objective To investigate the effects of ERK inhibitor PD98059 on cardiac energy metabolism and myocardial ischemia reperfusion injury in rats after cardiac arrest / cardiopulmonary resuscitation (CA / CPR). Methods Thirty-six rats were randomly divided into three groups: Sham group (n=6), PD98059 (PD) group (n=15) and model (CA) group (n=15). Rat model of CA/CPR in PD and CA groups was established by induction of ventricular fibrillation (VF) by electrical stimulation of the esophagus. Sham group was given operation only. After the restoration of spontaneous circulation (ROSC), PD group was given intravenous injection of PD98059 (0.3 mg / kg) immediately, CA group was given the same amount of normal saline. Survival was observed for 24 h. Serum samples were collected 24 h after resuscitation to detect troponin I. Meanwhile, myocardial tissue samples were collected for hematoxylin-eosin (HE) staining and ATP content determination. Western blot assay was used to detect the level of ERK and phosphorylation of ERK (p-ERK). Results After 24 h, the survival was 6 for Sham group, 6 for CA group and 13 for PD group. The serum level of troponin I was increased in CA and PD groups than that of Sham group, and which was decreased in PD group than that of CA group (P＜ 0.05). The cardiac tissue ATP content was significantly higher in PD group than that of CA group (P＜0.05), and the degree of myocardial pathological injury was significantly less in PD group than that of CA group. Compared with Sham group, the expression of myocardial p-ERK was significantly increased in CA and PD groups. The expression of myocardial p-ERK was significantly decreased in PD group than that of CA group (P＜0.05). Conclusion The treatment with ERK inhibitor PD98059 can improve the myocardial energy metabolism dysfunction and alleviate the myocardial ischemia reperfusion injury after cardiopulmonary resuscitation.

Key words: cardiac arrest, cardiopulmonary resuscitation, ischemia reperfusion injury, energy metabolism