Effect of mild hypothermia on the oxidative stress induced myocardial injury after cardiopulmonary resuscitation

Abstract

Objective To observe the effects of mild hypothermia on the myocardial mitochondrial injury induced by oxidative stress after restoration of spontaneous circulation (ROSC) in rat of cardiac arrest model. Methods Eighteen male Wistar rats were randomly(raudom number)divided into normal temperature group and mild hypothermia group after ROSC. Ultrasound was used to measure the left ventricular ejection fraction (EF), shortening fraction (FS) and stroke volume (SV). The levels of glutathione (GSH), malondialdehyde (MDA) and adenosine triphosphate (ATP) in myocardium were detected. The ultramicroscopic structure of myocardial mitochondria was observed under transmission electron microscope at 4 h after ROSC. Results There were no significant differences in basic life support (BLS) time, dosage of epinephrine and number of defibrillation attempt between two groups (P > 0.05). The concentrations of GSH and ATP in myocardium of rats in hypothermia group were significantly higher than those in normal temperature group, while the level of MDA was significantly lower in hypothermia group than that in normal temperature group. Echocardiographic findings showed that hypothermia could significantly improve the EF, FS and SV after ROSC. The hypothermia decreased the myocardial mitochondria injury rather than normothermia[mitochondrial injury score: (0.21±0.04) vs.( 0.42±0.08), P<0.05]. Conclusions In this model, mild hypothermia can decrease myocardial oxidative stress injury, improving the cardiac function after ROSC. Key words: Cardiac arrest; Cardio-pulmonary resuscitation; Mild hypothermia; Ventricular fibrillation; Cardiac function; Oxidative stress; Myocardial mitochondria; Rats