The Study Of Brain Death On The Myocardium Injury In The Wuzhishan Mini Pigs

Objective: Patients with brain death as sources of organ transplantation,Organs in the body tissues produced a series of complex changes at the state of brain death,Resulted in donor organ function damage or loss of a risk factor.Pathological reaction of different organs at the state of brain death,is the focus of the study of organ transplantation,it generates a series of athophysiological changes,can affect the quality of organs,thereby affecting the effect after transplantation.However,the organ injury after brain death mechanism is not yet clear,at present,brain death effects on cardiac function mainly related to the field of neural source of shock and release of inflammatory mediators and free radical,calcium overload and excess beta receptor free activation,hormone regulation.Myocardial enzyme is a marker of myocardial injury or necrosis,in which CK,CKMB and LDH is the enzyme markers commonly used in clinical myocardial activity on behalf of.Creatine kinase(Creatine Kinase,CK),heart muscle and brain tissue usually found in animal cells and mitochondria.The hybrid(MB)mainly in myocardial cells,myocardial damage or necrosis of myocardial enzyme contents will show different speed and different phase.The purpouse of this paper is established in Wuzhishan miniature pig brain death model through slow intracranial pressure and research the effect of ECG in the state of brain death with the change in time and myocardial enzymes in different brain death time trends,explore brain death after cardiac injury and its mechanism,to the brain dead organ donor evaluation and organ function and maintenance to provide experimental basis.Methods: 16 mini pigs were randomly divided into experimental group and control group.Experimental group was used to establish brain death model by intracranial pressure method,monitor ECG changes before and after brain death,1H before brain death and 0h,3h,6h,12 h after brain death,The changes of serum creatine kinase(CK),creatine kinase isoenzyme(CKMB)and lactate dehydrogenase(LDH)levels in 0h,3h,6h,12 h before and after brain death and brain death were also monitored and Ultrastructural changes of 12 h myocardium after brain death.The control group were treated by craniotomy without intracranial pressure.Results:1 ECG amplitude decreased and T wave amplitude increased with the time of brain death prolonged in the experimental group.2 CK value of the experimental group higher than the control group in 0h,3h,6h three time points,the difference between the two groups was statistically significant(P < 0.05),and the other time points were not statistically significant(P > 0.05).After brain death,CK value in the experimental group were all higher than those of the brain before death in 0h,3h,6h,12 h.(P < 0.05),and the CK value of the control group had no significant difference at different time points(P>0.05).3 CKMB value of the experimental group higher than the control group in 6h,12 h two time points,the difference between the two groups was statistically significant(P < 0.05),and the rest of the time points were not statistically significant(P > 0.05).After brain death,CKMB value in the experimental group were all higher than those of the brain before death in 0h,3h,6h,12 h.(P < 0.05).and the CKMB value of the control group had no significant difference at different time points(F=1.315,P=0.298).4 at each time point,the difference of LDH value between the two groups was not statistically significant(P > 0.05),the difference was not statistically significant(LDH,P=0.126)at different time points in the experimental group(F=2.315,P=0.126).In the control group,there were significant differences in LDH values at different time points(F=3.273,P=0.025),and the LDH values at 0h,6h and 12 h time points were all lower than those before operation(P<0.05).5 Brain death after 12 h myocardial ultrastructure showed dissolution of transverse fracture of disappeared,nuclear swelling,mitochondrial ridge partly dissolved and disappeared,some myofibrils were broken or disappeared,sarcoplasmic swelling,vascular endothelial swelling,basement membrane was not obvious,edema change tube,And compared with the control group,the sarcomere,nucleus,mitochondria,sarcoplasmic reticulum and vascular endothelial no obvious change.Conclusions:1 Wuzhishan-mini pig brain death model can be successfully established by the slow intracranial pressure method.2 Wuzhishan miniature pig brain death will cause myocardial damage,the performance for the different ECG specific changes and myocardial enzyme of elevated.3 myocardial ultrastructure was damaged after brain death.