The Roles Of ET-1, CGRP, TXA₂/PGI₂ In Delayed Cerebral Vasospasm Following Craniocerebral Trauma

Objective:To study the roles of ET-1,CGRP,TXA₂/PGI₂ in cerebral vasospasm following craniocerebral trauma so as to provide the theoretical and experimental data for exploring the mechanism of cerebral vasospasm following craniocerebral trauma, controlling the cerebral vasospasm following craniocerebral trauma and improving the prognosis of heavy craniocerebral traumatical patient.Methods:Forty-eight four-months-adult-rabbits were used to develop the mid-heavy craniocerebral traumatical animal model by the device of hydraulic pressure percussion to simulate the developing course and change of cerebral vasospasm in clinical patients.The blood flow velocity of the basilar artery of each rabbit were measured by transcranial doppler(TCD) in before trauma,on day one,day 3,day 7 after trauma.The blood was drawn from the heart and the cerebrospinal fluid was drawn from the cisterna magna(CM) to test the concentration of the ET-1,CGRP,TXA₂/PGI₂ by radioimmunity at the same time interval respectively.12 of the rabbits in the group were selected at random to operate the digital subtraction angiography(DSA) at the same time interval respectively.4 of the rabbits in the group were selected at random to operate the perfusion of internal carotid artery two sides,then the basilar artery was preserved for the pathological examination by the light and electronic microscopes.Results:The animal model was established successfully.After craniocerebal trauma, the animals showed twitch,change of muscle power of the left lower limb,lame,and reducement in the diet amount,weight and self cleaning ability.They recovered to the normal 2～3 days later.1.The peek speed of the basilar artery(BA) flow increased on day one,day 3,and day7 after trauma remarkably compared with before trauma(P＜0.05).The peek speed of the basilar artery flow increased on day3 after trauma more remarkably compared with dayl and day7 after trauma(P＜0.05),they showed high-peak,high-block,high-flow frequency spectrum.The shape and Vp,Vm of the BA in 7^th day after trauma were similar with on day one.2.The DSA study revealed that the blood vessel developed clearly,the time of the blood flow is normal before trauma.At the same interval after trauma,the DSA study showed the diameter of the BA decreased(P＜0.05),the branch of the blood vessel developed unclearly,the time of the cerebral blood flow prolonged,there is significant in the 3^rd day after trauma.3.The light microscopes study revealed:before trauma:the endothelium of the artery is slick,intimal elastic lamina(IEL) is no ruga,the smooth muscle cell arranged in order.After trauma:the wall of BA incrassated markedly intimal elastic lamina(IEL) showed ruga,the endothelial cell desquamated partly.The vascular smooth muscle revealed vacuolar degeneration, necrotic partly,the nuclear showed pyknosis.The membrane showed hyperplasy.The fibrocyte increased,granular cell and monocyte infiltrated.There is significant in the 3^rd after trauma.4.TEM displayed normal ultrastructural of blood vessel of the BA,morphology of EC,its conjunction,SMC and intimal elastic lamina(IEL) before trauma:while after trauma,noted pothological changes were observed,including desquamation and dystrophy of ECs,disruption of tight junction,vacuolated cytoplasm,condensation of chromatin in ECs,corrugation of IEL,distortion of SMC etal.It's showed similar with the early apoptosis expession of the cell,there is significant in the 3^rd after trauma..5.The change of the ET-1 in the blood isn't synchronal with the speed of the cerebral blood flow,but the change of the ET-1 in the CSF is synchronal with the speed of the cerebral blood flow. The CGRP in CSF and blood increased obviously in the forepart after craniocerebal trauma(1^st day),reached peek in the 3^rd day.The change of TXA₂PGI₂ is synchronal with the increase of the cerebral blood flow speed.The delayed cerebral vasospasm following craniocerebral trauma is correlation highly with the TXA₂/PGI₂ in CSF and blood.Conelusions:1.There is delayed cerebral vasospasm in the rabbit cerebral traumatic model induced by the the device of hydraulic pressure percussion.The model well mimicked the pathological changes of the cerebral vasospasm following craniocerebral trauma in hemodynamics,imageology,histopathology.It's a goood model to study the cerebral vasospasm following craniocerebral trauma.2.TCD is a safe measure to monitor persistently the cerebral flow,to discover the changes of the cerebaral blood-supply and the cerebral vasospasm.It's significant in the diagnosis and monitoration of the cerebral vasospasm following craniocerebral trauma.3.There is different morphologic changes of the vessel in the light microscopes and TEM study after CVS.The more heavily of the CVS,the more heavily of the injury of the vessel.4.It's not correlation with the ET-1 in blood in the delayed cerebral vasospasm following craniocerebral trauma.It may be correlation with the ET-1 in CSF.5.The CGRP in blood and CSF increased after craniocerebral trauma,but didn't rivalry the effect of vasoconstriction.6.The delayed cerebral vasospasm following craniocerebral trauma is correlation highly with the TXA₂/PGI₂ in CSF and blood.It might be the important reason of the delayed cerebral vasospasm following craniocerebral trauma.