| Objective:To observe the effects of mild hypothermia and cooling time on postresuscitation myocardial dysfunction,and further explore the partly underlying mechanism of action.Methods: After setting up rabbit model of cardiopulmonary resuscitation,30 rabbits were randomly divided into three groups.group A:normothermic resuscitation group,in which animals were performed standard CPR after cardiac arrest; group B:post-ROSC hypothermia group,in which animals were cooled to 32-34℃after successful ROSC; group C:intra-arrest hypothermia group,in which animals were cooled to 32-34℃before attempted resuscitation. The left ventricular end-diastolic pressure(LVEDP),left ventricular pressure rise and fall rate(peak±dp/dt), serum concentrations of H-FABP and 8-iso-PGF2a were observed. Results:compared with group A,the LVEDP,H-FABP and 8-iso-PGF2a of the remaining groups decreased singnificantly(P<0.05),the peak±dp/dt increased singnificantly (P<3.05);Increases of LVEDP,H-FABP and 8-iso-PGF2a in group C were less than in group B(P<0.05),wheras peak±dp/dt in group C were higher than in group B(P<0.05) at the same stage. Conclusions:mild hypothermia affords a significant cardioprotective effect,especially early intra-arrst cooling appears to be significantly better than post-ROSC cooling or normothermic resuscitation.The cardioprotective effect is possible associated with the reduction of 8-iso-PGF2a. |