Abstract 2409: Therapeutic Hypothermia Improves Postresuscitation Myocardial Dysfunction in an Asphyxia-Induced Cardiac Arrest Model
Introduction: Postresuscitation myocardial dysfunction, mostly resulting from ischemia-reperfusion injuries, is an unsolved issue in the resuscitation medicine. Organ protection is important during and even in the postresuscitation period. Hypothermia has been found to improve the postresuscitation neurological function and survival. However, its effects on the cardioprotection remain unclear.
Hypothesis: Therapeutic hypothermia can improve postresuscitation myocardial dysfunction.
Methods: Asphyxia-induced cardiac arrest was performed in male adult Wistar rats. Cardiopulmonary resuscitation including chest compressions, mechanical ventilation and epinephrine (0.01 mg/kg) was begun after 6.5 minutes of asphyxia. Hypothermia was induced by the icy saline gastric lavage with external cooling by ice packing after resuscitation. The target temperature 30 C was achieved within one hour after return of spontaneous circulation, maintained for 1.5 hours and then went to the passive rewarming process. The body temperature of control group was maintained within 36~37° C during the whole process
Results: The 4-hour survival rates were 38.5 % in control group and 82.6% in hypothermia group (P< 0.01). The left ventricular systolic function by dP/dt40 and diastolic function by maximal - dP/dt were better in the hypothermia group since 30 to 120 minutes after ROSC resuscitation period (p<0.05 for both). Less myocardial damage showed by the lower serum level of heart-type fatty acid binding protein in the hypothermia group at 4 hours after resuscitation (186.5 ng/ml in normothermia vs. 52.4 ng/ml in hypothermia group, p = 0.021). The eNOS was more expressed and prosurvival kinase Akt and ERK were more activated in the hypothermia group at 2 hours after ROSC.
Conclusion: Post-resuscitation hypothermia therapy is beneficial to post-resuscitation myocardial dysfunction and improves short term survival for the asphyxia-induced cardiac arrest. Its cardioprotective effects may be through the activation of prosurvival kinase and eNOS expression.