| Background: Head injury is one of the most commonly seen diseases in neurosurgery area,which threaten life of human and lead to very high mortality rate and disability rate. It was reported that the mortality rate of severe head injury is between 35-50%. One of important reasons resulting high mortality rate is secondary brain injury ,SBI after head injury. One of main manifestations of SBI is cerebral edema which is one of the most serious complications after head injury, cerebral edema can promote intracranial pressure and lead to malposition of brain tissue, even endanger life because of brain hernia. In recent year, following the further study about head injury and cerebral edema, the role cytokine and selfinjurying substance act in head injury more and more become focus of study at present. Under normal condition, the content of cytokine in human body is few, but expression of which could rapidly increase if stimulated by various kind of factors such as infection, trauma, ischemia, tumor, hemorrhage. The type of cytokine is plenty, they act as different roles in inflammation reaction, chances are that they participate various pathological and physiological reaction after head injury, for example fever, leucocyte aggregation, increasing permeability of blood vessel endothelial cell and reaction in acute stage. Among the total cytokine, TNF-α and IL-1βparticipate occurrence of head injury and brain edema. Their transient excessive expression in earlier period after injury is important factor resulting in SIB. In addition, after head injury in brain emerge a great deal of selfimpairing materials that could injury brain cell, destroy blood brain barrier, induce and aggravate head injury,brain edema and so on. Nowadays what are mainly studied include: excitatory amino acids,bradykinin,catechol amine,free radical(NO,O2- ,etl),Ca2+ ,endogenous opioid peptides and so on. To use corresponding antagonist or free radical cleaner could effectively protect brain cell, relieve cerebral edema and head injury. Therefore, it is key point to inhibit develop of cytokine and selfimpairing substance earlier in treating head injury.objective: this experiment studys dynamic change of TNF-α,IL-1β,NO in cerebral tissue and relation between head injury and cerebral edema with model of brain injury of rat.Methods1.object42 adult male Sprague-Dawley(S-D) rats(provided by animal experiment center of Dalian Medical University) with 250~300g of weight. That are divided into seven groups: normal group(N),spurious injury group,4h after trauma(T4 ),8h(T8),24h(T24),72h(T72),168h(T168), six rats per group.2.methodTo make closed cerebral trauma model of rat by using method of Feeney`s epidural strike with free drop body. To check content of cerebral water,TNF-α,IL-1β,NO individually and dynamically with methods as dry-wet SG,indirection,radio-immunity.Results:The contents of above-mentioned three materials all rise obviously after cerebral injury, but time when peak occurs is different. Content of IL-1βin cerebral tissue beside injury point apparently rises 4 hours after injury; content of NO in cerebral tissue begins to rise and achieves peak in 8 hours; contents of water and TNF-αin cerebral tissue apparently rise 4 hours after injury and achieve peak in 24 hours.Explanation for result of correlation analysiscontents of water and NO in cerebral tissue are positive correlation(r =0.382,p﹤0.05), TNF-αand NO; TNF-αand IL-1β; IL-1βand NO are all obviously positive correlation.(r =0.497.r =0.665.r =0.646,p﹤0.01). the content of water in cerebral tissue is obviously positive correlation with TNF-αand IL-1β(r =0.703,r =0.554,p﹤0.01).discussion:cerebral edema is a key point factor to endanger life, there are many reasons to result in cerebral edema. With the develop of neuroimmunology, actions of cytokine and selfimpair substance in cerebral edema are already paid great attention. Nowadays cytokine is deemed to attend formation of cerebral edema. The most important cytokin... |
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