| Objectives:The recovery of cerebral function is an effective evaluation measures for the Cardiopulmonary Resuscitation (CPR). How to reduce the injury of the brain function effectively after cardio arrest (CA) and CPR becomes the hot point. CA and CPR had a complex mechanism of brain reperfusion injury. Oxygen free radicals and the series of consequences are the main harmful effects on brain after reperfusion. The oxygen free radicals damage the brain by the lipid peroxidation which oxygen free radicals and brain unsaturated fatty acid tissue occurred and the proteins and DNA oxidative damage. Also the Secondary reaction included metabolic products which contracted the cerebral blood vessels and reduced local blood flow, calcium overload, inflammation aggravate ischemic brain damage further. Tea polyphenols had strong antioxidant effect and could prevent the oxidizing reaction by its phenolic hydroxyl group combined of oxygen free radicals and lipid peroxides. Its protection of the brain was confirmed in the cardio cerebral ischemia reperfusion study. The process of CPR and CA could cause the cerebral ischemic reperfusion in the same extent, thus it also lead to reperfusion injury. Whether tea polyphenols protect the brain after CPR remains unclear.Based on the above reasons,this experiment was to testify whether tea Polyphenols protect the brain through the enhancing effect of Superoxide Dismutase (SOD) and reduce the yield of Malondialdehyde (MDA) generated by Lipid oxide in an asphyxia rat model after being treated with Tea Polyphenols intravenously following ROSC。Methods:1. Eighty-four Sprague-Dawley rats, weighing 220-440 g, were anesthetized by intraperitoneal injection of 3ml/kg Chloral Hydrate. A 14-gauge cannula was inserted orally. Cardiac rhythm was monitored with a standard lead II ECG. A PE-50 catheter was advanced into the left formal vein for drug treatment. Another PE-50 catheter was advanced into the left formal artery for measurement of aortic pressure. Asphyxial cardiac arrest was induced by clamping the tracheal tubes. Cardiac arrest was determined by loss of aortic pulsations and mean aortic pressure< lOmmHg. At the end of 8 min of asphyxiation, CPR was started. Ventilation was performed with a volume-controlled small animal ventilator (ALC-V9, Shanghai Alcott Biotech CO. LTD, China), with room air at 70 breaths per min and tidal volume adjusted to 6 ml/kg. Mechanical chest compression was performed at a rate of 180 compressions per min with equal compression-relaxation duration. Epinephrine was treated at 1 min of compression. Restoration of spontaneous circulation (ROSC) was defined as the return of supraventricular rhythm with a mean aortic pressure of> 20mmHg for a minimum of 5min. Resuscitation efforts were discontinued in case failing to restore spontaneous circulation at 5 min following the initiation of CPR. The animals were intravenously treated randomly with either saline (Sal-gro, n=40) or lOmg/kg tea polyphenols (Tp-gro, n=40) following ROSC. The changes of Systolic Pressure (SBP)、diastolic pressure (DBP)、mean arterial pressure(MAP)were monitored after an hour of ROSC. Survival time, neurological deficit score (NDS) and the survival rate were recorded after 12,24 and 48 h of ROSC respectively.2. Forty-five Sprague-Dawley rats, weighing 240-440g, were randomly into 3 groups, n= 15, sham group (Con-gro), saline group (Sal-gro), tea polyphenols group (Tp-gro), then each accord the 12h,24h,48h three time points divided further three groups. The asphyxia rats’model of cardiac arrest was the same as part one. Rats were intravenously treated immediately with either saline (Sal-gro, n=15) or 10mg/kg tea Polyphenols (Tp-gro, n=15) following ROSC. Rats were taken at each time point of blood, brain for collecting specimens. The rat dead before the execution phase was exited the experiment. It would take another supplement. It would make sure in the execution phase there were 5 rats per group. In sham groups, rats were only treated femoral artery, vein and surgical endotracheal intubation and the line of ECG, blood pressure monitoring, did not induce asphyxia and do the CPR. The changes of SOD, MDA in serum were assayed and brain hippocampal pathological changes were observed with the set point 12h,24h,48h respectively.Results:1. There was no significant difference in SBP, DBP, and MAP within one hour of post-resuscitation in the TP group and the Saline group. The survival time of rats in TP group was significantly longer than that of in saline group (37.3±11.2hvs24.3±14.1h, P<0.05),24h and 48h survival rates in TP group after ROSC was also significantly higher than the saline group (P <0.01), and the 24h,48 h NDS score also significantly higher (P<0.05).2. The blood SOD of 24h,48h after ROSC was significantly higher in TP group than in saline group (P<0.05), the blood MDA of 12h,24h,48h time was significantly less in TP group than in saline group (P<0.05 or P<0.01). There was no significant difference of brain hippocampus pathologic between the two groups at 12h point, while at the 24h and 48h, rats of the saline group had more necrosis neurons than that of TP group.Conclusion:1. Tea polyphenols ensured a prolong survival time of the rats as well as which also reduced neurological damage after cardiopulmonary resuscitation in asphyxia models.2. TP increased the serum activity of SOD, inhibited the reaction of lipid metabolism and alleviated the injury of cerebral pathology after CPR in an asphysixal rat model. |
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