Role of JNK signal pathway in brain injury after resuscitation in a rat model of asphyxia cardiac arrest
10.3760/cma.j.issn.0254-1416.2012.01.024
- VernacularTitle:JNK信号通路在大鼠窒息性心跳骤停复苏后脑损伤中的作用
- Author:
Long CHEN
;
Mingzhang ZUO
;
Gongjian LIU
;
Xiyan CHEN
;
Yan ZHANG
;
Qin CHENG
;
Maoyin ZHANG
- Publication Type:Journal Article
- Keywords:
JNK mitogen-activated protein kinases;
Asphyxia;
Heart arrest;
Brain injuries
- From:
Chinese Journal of Anesthesiology
2012;32(1):93-95
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the role of JNK signal pathway in brain injury after resuscitation in a rat model of asphyxia cardiac arrest.Methods Forty healthy male SD rats 'weighing 300-350 g were randomly divided into 4 groups ( n =10 each):sham operation group (group SH) ; cardiac arrest group (group CA) ; group SP600125-JNK inhibitor (group SP) and dimethyl sulfexide (DMSO) group.The rats were anesthetized with intraperitoneal pentobarbital 45 mg/kg,tracheostomized and mechanically ventilated.PETCO2 was maintained at 35-45 mm Hg.Femoral artery and vein were cannulated for BP monitoring and fluid infusion.Cardiac arrest was induced by clamping tracheal tube until ECG activity disappeared and MAP < 10 mm Hg.Resuscitation was started at 3 min after cardiac arrest.MAP > 60 mm Hg and HR > 250 bpm were considered to be signs of successful resuscitation.SP600125 20 mg/kg and DMSO 0.2 ml were injected iv as soon as chest compression was started in groups SP and DMSO respectively.The animals were sacrificed at 5 h after successful resuscitation and their brains were removed for determination of wet/dry (W/D) weight ratio and microscopic examination of hippocampus.Neuronal apoptosis was detected by TUNEL.Results Cardiac arrest significantly increased W/D ratio and the number of apoptotic cells in group CA.SP600125 iv significantly attenuated the cardiac arrest-induced increase in W/D ratio and the number of apoptotic cells but DMSO did not.Conclusion JNK signal pathway is involved in the brain injury after resuscitation in a rat model of asphyxia cardiac arrest.