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