The Study Of The Bosentan's Effect On The Basilar Arteries And Apoptosis Protein Of Rats After Subarachnoid Hemorrhage

Purpose: To establish the subarachnoid hemorrhage model of ratsby double injections of blood into cistern magna. To find the effect ofBosentan in the basilar arteries and the apoptosis protein of subarachnoidhemorrhage(SAH) rats.Methods: Established the subarachnoid hemorrhage model of ratsby double injections of blood into cistern magna. The thirty healthy SD(250g±15g) rats were randomly divided to three groups: A.shamoperated; B. subarachnoid hemorrhage (fed the same volume ofisotonic saline); C. Bosentan group (fed Bosentan 100 mg/kg·d afterSAH). Each group was made up by ten rats. All groups were sacrificed atthe 7th day after operation and get the basilar arteries for HE stain. Thenthe diameters and the thickness of vessel wall were measured. All thebrain slices were examined. The morphological changes of the neurons inhippocampal formation were observed by HE stain.Immunohistochemistry was used to quantitatively determine theexpression levels of Bcl-2 and Bax by means of cell counting andimaging system.Result: 1. The comparison of the diameters and thickness of vesselwall of basilar arteries in each group: There were statistical significancebetween A and B, B and C and A and C, which means the Bosentan can relieve the vasospasm of basilar arteries after SAH.2. The observation of HE stained hippocampal formation inlight microscope: There were differences of the neuronic morphologybetween A, B and C.3. The comparison of expression levels of Bcl-2 and Bax inhippocampal neurons of each group: There were statistical significancebetween A and B, B and C and A and C, which means the Bosentan canrelief the increase expression of Bax and the decrease expression of Bcl-2in neuron of hippocampal formation after SAH.Conclusion: Bosentan can improve the blood supply of the brain byrelieving the cerebral vasospasm of the basilar arteries after subarachnoidhemorrhage, which results in interruption to the increase expression ofBax and the decrease of Bcl-2 in hippocampal neurons, then protect theneuron by decrease the apoptosis of the hippocampal neuron.