The No Level Post On ASAH Phase Of Change And The Relationship Between Early Brain Injury

Spontaneity subarachnoid hemorrhage(subarachnoid hemorrhage, SAH) are many causes of traumatic brain caused by non-bottom surface of vascular rupture or cerebral spinal, Direct inflow of blood due to an acute subarachnoid hemorrhagic cerebrovascular disease, it is the most common one of cerebrovascular accident, mostly with aneurysmal subarachnoid hemorrhage (aneurysm subarachnoid hemorrhage, aSAH)Clinical findings, nitric oxide in acute subarachnoid hemorrhage (nitric oxide, NO) increased the level of direct and illness, prognosis and recurrence, speculated that NO may be an early brain injury after subarachnoid hemorrhage play a key role. However, the acute phase after SAH cerebrospinal fluid and plasma NO levels change? NO in the early brain injury after subarachnoid hemorrhage is how to play a role? Answers to these questions is unclear.Objective:Spontaneous subarachnoid hemorrhage in rabbits after the establishment of the early symptoms of brain injury model, the phase of the observed changes in NO and the relationship of early brain damage, for further study of NO early after subarachnoid hemorrhage in the brain injury mechanism The basis of theoretical basis.Methods:1. cisterna magna through a method of injecting autologous arterial blood, the establishment of rabbit early symptoms of brain injury model of subarachnoid hemorrhage;2. by Endo IV classification, after the model of rabbits to rate behavioral changes;3. NO by nitrate reductase assay content, rendering NO content in plasma and cerebrospinal fluid phase curve;4. by light and electron microscope pathological changes in the temporal lobe of the cerebral cortex.Results:1. Rabbit cisterna magna puncture after the first injection of autologous blood can be successfully established symptomatic SAH model of early brain injury;2. In this model, the experimental group and the subarachnoid cistern found a lot of blood clots and blood, after obvious symptoms of neurological behavior. Neurological score of the experimental group and control group were significantly different.3. The naked eye:the experimental group were seen after modeling a large number of blood clots or blood distribution in the subarachnoid space, and no brain parenchymal damage; control group and the control group were normal.4. Cell morphological changes:edema of nerve cells, some neurons stain unevenly stained, condensed, light staining, showing typical apoptotic and necrotic neurons; control group and the control group showed no definite abnormality. Electron microscope showed vacuolar changes in glial cells, neurons deformation, increase in nuclear heterochromatin, power density increased, the nuclear membrane and the nucleus ambiguous gap. Control group and the control group showed no change.5. NO concentration in plasma and cerebrospinal fluid changes in the characteristics: After modeling 12h:experimental group and control group and the control group there were significant differences (P<0.01); after the model 4h,24h,48h,72h:the experimental group and control group and blank group no difference. After modeling the experimental group, NO concentration in a certain phase changes in time:after the model was significantly increased 12h,72h after the return to levels before modeling; control group and the control group after the modeling phase of no changeConclusion:1. Through a cistern autologous blood injection method is a simple and repeatable model of SAH in early brain injury.2. After the success of the animal model, there has been significant damage in neurological behavior performance and a certain phase of the changes of time; cortex staining, cortical neurons appear hypoxic expression, nerve cell necrosis and apoptosis-like changes and further that this model is suitable for the study of early brain injury in the pathogenesis.3. Successful construction of the model detected after plasma and cerebrospinal fluid concentration of a certain time NO changes phase, after the success in modeling the highest concentration 12h,72h returned to normal, and nerve injury in the performance of behavior relative to the presence of sexual relations. After the aSAH that NO play a role, NO concentration in a certain extent can explain the extent of neuronal cell injury...