Abstract
Objective To investigate the role of gap junction in the pathomechanism and treatment of cerebral vasospasm after experimental subarachnoid hemorrhage.Methods HE dyed was used to identify the model.The diameters of basilar arteries were determined by pressure myograph.The connexins in the basilar arteries of different groups were examined by western blot.Results The diameters,connexins in basilar arteries were compared in and between groups respectively.There are more significant differences in operation group compared with control,sham and treatment group(P ＜ 0.01),that is Cx40 and basilar arteries diameters are reduced,Cx43 and Cx45 are elevated.But the differences in and between Control,sham and treatment group are not obvious (P ＞ 0.05); Cx37 can't examined; Cx40 and basilar arteries diameters are positive correlation(P ＜0.01,r =0.823),with Cx43 and Cx45 are negative correlation(P ＜0.01,r =-0.840; P ＜0.01,r =-0.839).Cx43 and Cx45 with basilar arteries diameters are negative(P ＜0.01,r =-0.828;P ＜0.01,r =-0.823).Cx43 and Cx45 are positive correlation(P ＜ 0.01,r =0.939).Conclusions Cx43 and Cx45 proteins play an important role which is promotion in the pathomechanism of cerebral vasospasm after experimental subarachnoid hemorrhage,but Cx40 is opposite; There are correlation among Cx40 and Cx43 Cx45,Cx43 and Cx45 are positively correlated,Cx40 and Cx43,Cx45 are negatively correlated,respectively.Gap junction inhibitor 18β-glycyrrhetinic-acid can relieve cerebral vasospasm after experimental subarachnoid hemorrhage in rats in vivo. Key words: Subarachnoid hemorrhage ; Cerebral vasospasm; Gap junction; 18β-glycyrrhetinic-acid
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