| Part One:Objective To establish a stable rat model of asphyxia cardiac arrest by clamping endotracheal tube.Methods A total of 30 clean male Sprague Dawley rats,weighing 200?300g,catheter were inserted into arteries and venous after anesthesia and tracheal intubation,with maintaining stable circulation and ventilation.At end-expiratory by clamping the endotracheal tube set up cardiac arrest after model,cardiopulmonary resuscitation after the Systolic blood pressure was lower than 25 mmHg 5 minutes later.Results After clamping the endotracheal tube(266.58±40.28)s,rats were cardiac arrest,28 examples succeed,and 2 examples fail,success rate 93.3%.Conclusion The model is stable,easy to be operated,can meet the needs of the subsequent experimental studies.Part Two:Objective To investigate the degree and the mechanism of brain damage induced by cardiac arrest and resuscitation in rats.Methods 16 male Sprague Dawley rats were randomly divided into the Sham group and Cardiac arrest/Cardiopulmonary resuscitation(CA/CPR)group.The model of cardiac arrest induced by asphyxia were established and CPR was performed.Serum protein NSE,S00O? were detected by ELISA method.The levels of bax,bcl-2,caspase-3 protein were measured by Western Blot.Neuronal apoptosis were detected by TUNEL method and observed morphological changes of rat brain.Results Compared with Sham group,S100? in CA/CPR group was higher at 0h,3h,6h after resuscitation,and the difference was statistically significant(P<0.05).The levels of NSE in CA/CPR group were higher than that in Sham group at 6 hours after resuscitation,and the difference was statistically significant(P<0.05).CA/CPR group of serum protein NSE,S00O? was rising,S100? protein levels was statistically significant(P<0.05).Compared with Sham group of bax,caspase-3,bcl-2,CA/CPR group of bax,caspase-3 protein become high,but bcl-2 is reduced,and the difference was statistically significant(P<0.01).The apoptosis rate of neurons in CA/CPR group was higher than that in Sham group(P<0.01).The change of brain tissue morphology was more obvious in CA/CPR group.Conclusion Five minutes of cardiac arrest in rats causes significant damage to brain tissue,and gradually increased.It may trigger apoptosis mechanism.Part Three:Objective To study the effects of different ischemic strategies on the brain injury in rats with cardiac arrest.Methods Forty male Sprague Dawley rats were randomly divided into Sham group,cardiac arrest/cardiopulmonary resuscitation group(CA/CPR),remote ischemic preconditioning group(RIPC),remote perconditioning group(RPC)and remote ischemic post-conditioning group(RI-PostC).Serum protein NSE,S100? were detected by ELISA method.The levels of bax,bcl-2,caspase-3 protein were measured by Western Blot.Neuronal apoptosis were detected by TUNEL method and observed morphological changes of rat brain.Results Compared with CA/CPR group,The levels of S100? in RIPC group were higher at Oh,3h,6h after resuscitation,the levels of NSE were higher in RIPC group at 6 hours after resuscitation,and the difference was statistically significant(P<0.05).The expression of bax and caspase-3 in RIPC group and RI-PostC group were lower than those in CA/CPR group(P<0.05),and the expression of bcl-2 was higher than those in CA/CPR group(P<0.05).The expression of caspase-3 in the RIPC group was lower than that in the RI-PostC group(P<0.01).The apoptosis rate of hippocampal neurons in ischemic preconditioning group was significantly lower than that in CA/CPR group(P<0.01),and the apoptosis rate was the lowest in RIPC group.The changes of brain morphology were more obvious in CA/CPR group,and the brain injury in ischemic preconditioning was lighter.Conclusion RIPC and RI-PostC can effectively reduce the brain injury by suppressing cell apoptosis in cardiac arrest model,the RIPC group of brain protective effect is slightly better,it may be related to inhibition of endogenous apoptpsis in the mitochondrial pathway. |
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