Cardiopulmonary Resuscitation Hypothermia On Cerebral Protection Mechanism

Objective:Therapeutic hypothermia after resuscitation can reduce ischemia-reperfusion injury, and has been included in cardio-pulmonary resuscitation guidelines. But hypothermia treatment programs is not perfect, reduce cell damage and apoptosis molecular mechanism is not clear. Therefore required further study provide important scientific theoretical basis for the wide range of clinical applications, and thus may provide new therapeutic targets for the protection of ischemia-reperfusion injury.Methods:Sixty healthy male SD rats that achieved return of spontaneous circulation (ROSC) after a7-9-min asphyxial cardiac arrest were block randomized to normothermia (36-37℃) or TH (30-34℃) initiated0,2,6,12or24hours after ROSC and maintained for12hours. Rats’ neurologic deficit score (NDS) and brain water content (BWC) were measured, brain tissue pathological changes and TUNLE staining rat brain cell apoptosis were observated. AIF、caspase-3、Fas mRNAgene expression level of rat brain was detected by RT-PCR.Results:Hypothermia group compared with the normothermia group rats12and24hours neurological deficit scores were high (P<0.05),6and12hours brain water content decreased (P<0.05), H&E stained pathological6and12hours brain edema significantly reduce, TUNEL results showed that the number of6,12and24hours brain cell apoptosis decreased (P<0.05), AIF、caspase-3、Fas mRNA gene expression was significantly reduced at each time poit.Conclusion:Therapeutic hypothermia after resuscitation can improve neurologic deficit score (NDS), cerebral edema; through inhibition of brain tissue AIF、caspase-3、Fas mRNA expression of apoptotic genes play a role in brain protection.