| Background and Objectives: The research of cardiopulmonary resuscitation (CPR) is a focus in emergency and critical care medicine. At present time,the mortality after CPR is still high. Cardiac arrest patients, after CPR, will inevitably have their internal organs all over the body damaged due to ischemia reperfusion, which leads to the secondary damage of the internal organs. Brain tissue is especially sensitive to hypoxia or ischemia. There will be permanent brain damage if cardiac arrest time is over 5 minutes at normal temperature. And the recover of brain function isn't satisfactory. The cerebral resuscitation is an important factor which determines the success rate of CPR.In recent years, great progress was made in the pathophysiology mechanism of cerebral resuscitation, and it provided the theory basis for treatment of cerebral resuscitation. After CPR, the damage to brain tissue occurred consequently due to hypoxia, such as brain edema, ischemia reperfusion injury. The pathophysiology mechanism of ischemia reperfusion was complicated, including the formation of large quantity of free radicals during ischemia reperfusion, disturbance of brain cell energy metabolism, intracellular calcium overload and activation of human immune system. Inflammatory response took an important part in ischemia reperfusion injury. Acute inflammatory response characterized by the release of inflammatory mediators reinforced is ischemia reperfusion injury.Microparticles (MPs) are circulating, phospholipids rich, submicron particles released from the membranes of endothelial cells, platelets, leucocytes and erythrocytes. It has been reported that microparticles are tight related with microvascular thrombosis, vascular disorders and inflammation, for example coronary artery disease, severe hypertension or arteriosclerosis. While investigation into their biological activity has revealed diverse actions in cell signaling, apoptosis and activation.The method of clipping trachea to asphyxia is used in this study to reproduce the cerebral resuscitation model of global cerebral ischemia and hypoxia injury in rats. The model is comparable to the patients with cerebral resuscitation. The content of inflammatory factor in serum and supernatant fluid of cerebral tissue were detected. The levels of microparticles (PMP, EMP) in plasma and water content in brain tissue were measured. To investigate the alterations of inflammatory factor and endothelial-derived and platelet-derived microparticles after cardiopulmonary resuscitation.Methods:The method of clipping trachea to asphyxia is used in this study to reproduce the cerebral resuscitation model of global cerebral ischemia and hypoxia injury in rats. The model is comparable to the patients with cerebral resuscitation. Sixty healthy SD rats, weight ranging from 270~320g, were randomly divided into control group and cardiopulmonary resuscitation group, each group has thirty rats. Control group was taken as false cardiac arrest group, no sideration needed to cause cardiac arrest after pretreatment. Cardiopulmonary resuscitation group was induced cardiac arrest and treated with standard CPR. The rats were scored and taken samples at immediate, 1 h, 2 h, 4 h and 8 h. After that, the content of TNF-α, IL-6 and IL-10 in serum and supernatant fluid of cerebral tissue were detected. The levels of microparticles (PMP, EMP) in plasma and water content in brain tissue were measured. The brain tissue also undergo histopathologic examination with HE staining.Results:(1) The serum and cerebral tissue content of TNF-αin the resuscitation group obviously increased at 1h after ROSC, and increased gradually with time prolonging and significantly higher than those in control group and prearrest (P<0.01). The serum level of TNF-αin control group didn't have significant change at immediate, 1 h, 2 h, 4 h and 8 h.(2) The serum and cerebral tissue content of IL-6 in the resuscitation group obviously increased at 2 h after ROSC, and increased gradually with time prolonging and significantly higher than those in control group and prearrest (P<0.01). The serum level of IL-6 in control group didn't have significant change at immediate, 1 h, 2 h, 4 h and 8 h.(3) The serum and cerebral tissue content of IL-10 in the resuscitation group obviously increased at 8 h after ROSC, and didn't have significant change at immediate, 1 h, 2 h and 4 h. The serum level of IL-10 in control group didn't have significant change at immediate, 1 h, 2 h, 4 h and 8 h.(4) The plasma content of microparticles (PMP and EMP) in the resuscitation group obviously increased at 1h after ROSC,and increased gradually with time prolonging and significantly higher than those in control group and prearrest (P<0.01). The plasma content of microparticles (PMP and EMP) in control group didn't have significant change at immediate, 1h, 2h, 4h and 8h.(5) The water content in brain tissue in the resuscitation group obviously increased at 1h after ROSC, and increased gradually with time prolonging and significantly higher than those in control group and prearrest (P<0.05 or P<0.01). The water content in brain tissue in control group didn't have significant change at immediate, 1 h, 2 h, 4 h and 8 h.(6) The NDS of rats in the resuscitation group obviously decreased at 1h after ROSC,and decreased gradually with time prolonging and significantly lower than those in control group and prearrest (P<0.05 or P<0.01). The NDS of rats in control group didn't have significant change at immediate, 1 h, 2 h, 4 h and 8 h.(7) There are positive correlation between the level of TNF-α, IL-6 and the parameters of water content in brain tissue, negative correlation between the level of TNF-α, IL-6 and NDS.(8) There are positive correlation between the level plasma of microparticles(PMP and EMP) and the parameters of water content in brain tissue, negative correlation between the level plasma of microparticles (PMP and EMP) and NDS.(9) Histological examination showed that normal pyramidal cells in hippocampal CA1 region showed round and pale stained nuclei in HE staining. Compared with control group, most neurons in CA1 region of hippocampus were eosinophilic degenerated and many shrunken cells with pyknotic nuclei which were counted as dead cells could be seen in ischemia reperfusion groups.Conclusions:(1) There was obviously cerebral ischemia reperfusion injury in the model of CPR rats. Water content in brain tissue obviously increased and NDS markedly decreased in the cerebral ischemia model with CPR rats. The injury of brain tissue with HE staining was obvious.(2) There are systemic inflammatory response syndrome (SIRS) in post-resuscitation rats after cardiac arrest which was associated with increases in expression of cytokines in cerebrum. The higher of serum and cerebral tissue content of TNF-α,IL-6, the heavier of cerebral ischemia reperfusion injury.(3) The mechanism of postresuscitation cerebral ischemia reperfusion injury might be related with unbalance of pre-inflammation cytokines (TNF-a and IL-6) and anti-inflammation cytokine (IL-10).(4) PMP and EMP participate in onset and development of cerebral ischemia reperfusion injury. There are relationship between the level plasma of microparticles (PMP and EMP) and cerebral ischemia reperfusion injury. |
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