Abstract： Objective To analyse the relationship between cytochrome C release and the opening degree of the permeability transition pore (PTP) during in post cardiopulmonary resuscitation(CPR) rats. Method Adult male Sprague Dawley (SD)rats were randomly (random number ) divided into a surgical sham group (no CA/CPR) ( n = 8) and CA/CPR group ( n = 48). Animals in CA/CPR group was induced by asphyxiation and icecold 0.5 mmol/L KCI and killed by decapitation and processed for isolation of brain cortex mitochondria at 3 h,6 h,12 h,24 h,48 h,72 h after restoration of spontaneous circulation (ROSC). MPTP opening degree was based on the absorbance changes of the mitochondrial suspension at 540 nm. Western blot analysed the release of CytC from mitochondrial to cytoplast. Results Neural cells MPTP always remained opening post ROSC. The opening degree of MPTP was not reaching the peak instantly. While its' change depended on time: remaining low level within 6 h post ROSC,then rapidly opening, till 12 h reaching the largest degree,and at 24 h post ROSC slightly shrunken. All these suggested that mitochondria started to shink. While at 48 h the opening degree largen again, shrunken once more at 72 h,but not reaching the normal level ( P ＜ 0.05 or P ＜ 0.01). Cytochrome C could not be detected in the cytosol in the earlier phases of the sham-operated brain samples but appeared in the mitochondria.The amount of cytochrome C released was proportional after restoration of spontaneous circulation 3 h and 24 h,failed to detect the enzyme in the mitochondria fraction. Conclusions We draw the conclusion MPTP plays a key role in neurocyte apoptosis after CA/CPR, which leads to mitochondria release CytC.