The effect of win55, 212-2 on neuronal apoptosis in post-resuscitation in rats / 中华急诊医学杂志

ABSTRACT

Objective To investigate the pharmacological hypothermic effect of WIN55, 212-2 on neuronal apoptosis after cardiopulmonary resuscitation. Methods Cardiac Arrest ( CA ) was induced in Sprague-Dawley rats.Five minutes after onset of CA, cardiopulmonary resuscitation ( CPR) was carried out.At 30 minutes post-resuscitation, the animals were randomized into three groups (n=10 in each group): (1) WIN55, 212-2 hypothermia group [W group, WIN55, 212-2, 1 mg/(kg· h)].(2) Normothermia group (NT group, 5%DMSO);(3) WIN55, 212-2 with normothermia group (W+NT group, WIN55, 212-2, 1 mg/(kg· h).Animals in WIN55, 212-2 hypothermia group and WIN55, 212-2 with normothermia group were dealt with continuous intravenous infusion of WIN55, 212-2 [1 mg/(kg· h)] for 4 h, while rats in NT group were infused with equal volume of 5% DMSO instead.The survival time and neurological deficit score ( NDS) were observed.The CA models were established in three groups.After rats were sacrificed, the brains were harvested for detecting histopathological changes and apoptosis of neural cell at 24 h, 48 h and 72 h after ROSC respectively.Five animals of each group were chosen randomly ( random number ) .Results Body temperatures of rats in W group decreased from 37°C to 34°C in 4 hours.Accumulated survival rate in W group was higher than that in the other two groups ( P=0.02) .NDS was significantly improved in W group than that in the other two groups ( P<0.05) .Morphological change in W group was less serious than that in the other two groups.The number of neuron apoptosis in W group was smaller than that in the other two groups.Conclusions WIN55, 212-2 inducing pharmacologically hypothermia during post-resuscitation prolonged survival and improved cerebral function in rat cardiac arrest models.The beneficial effects of WIN55, 212-2 were associated with ameliorating the histopathological damage in brain and alleviating the neuron apoptosis.