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目的 探讨缝隙连接阻断剂18β-甘草次酸对蛛网膜下腔出血后脑血管痉挛的治疗作用.方法 120只SD大鼠随机数字表法分对照组、假手术组、手术组及治疗组各30只,且各组分第1,3,5,7,14天5亚组,各亚组6只.视交叉前池二次注血法建立Sprague Dawley大鼠蛛网膜下腔出血动物模型,HE染色鉴定模型,大鼠神经行为学评分、Western blot检测脑血管Cx43表达及全细胞膜片钳技术观察缝隙连接通道电导率变化.结果 神经行为学评分显示,手术组第3,5,7,14天明显下降,分别为(8.33±0.38)分,(6.67±0.20)分,(4.83±0.31)分,(9.33±0.51)分,与对照组、假手术组比较差异有统计学意义(P＜0.01),不同时间点间比较差异有统计学意义(P＜0.01),治疗组第3,5,7,14天分别为(10.00±0.65)分,(10.17±0.66)分,(9.83±0.61)分,(10.67±0.70)分,与手术组比较差异有统计学意义(P＜0.01)；Cx43蛋白表达结果显示,手术组第1,3,5,7,14天明显升高,分别为(0.289±0.01)％,(0.389±0.008)％,(0.510±0.006)％,(0.651±0.019)％,(0.329±0.151)％,与对照组、假手术组比较差异有统计学意义(P＜0.01),不同时间点间比较差异有统计学意义(P＜0.01),治疗组第1,3,5,7,14天分别为(0.225±0.007)％,(0.228±0.01)％,(0.251±0.02)％,(0.303±0.008)％,(0.267±0.008)％,与手术组比较差异有统计学意义(P＜0.01)；电导率记录结果,手术组第1,3,5,7,14天明显升高,分别为(3.07±0.19) nS/m,(4.88±0.34) nS/m,(8.20±0.31) nS/m,(11.94±0.22) nS/m,(4.07±0.22) nS/m与对照组、假手术组比较差异有统计学意义(P＜0.01),不同时间点间比较差异有统计学意义(P＜0.01),治疗组第1,3,5,7,14天分别为(1.38±0.16) nS/m,(1.64±0.15)nS/m,(2.26±0.21) nS/m,(2.89±0.85) nS/m,(2.11±0.20) nS/m,与手术组比较差异有统计学意义(P＜0.01).结论 缝隙连接阻断剂18β-甘草次酸可明显缓解蛛网膜下腔出血后脑血管痉挛的发生,缝隙连接在蛛网膜下腔出血后脑血管痉挛的病理机制中起着重要作用.“,”Objective To investigate the role of gap junction in the pathomechanism and treatment of cerebral vasospasm after experimental subarachnoid hemorrhage.Methods 120 Spragne Dawley rats were assigned randomly to four groups: control(n=30),sham group(n=30),operation group(n=30) and treatment group(n=30).Animals were killed on the 1st,3rd,5th,7th and 14th day(n=6) respectively.The Spragne Dawley rat twosubarachnoid hemorrhage model was established by injection autogenous femoral artery blood into the front pool of optic chiasma.Neurologic deficit score were tested with Kaoutzanis M scale.lE dye was used to identify the model.The Cx43 proteins in the basilar arteries were detected by Western blot.Whole cell patch clamp technique was used to record the electrophysiological changes of gap junction channels in basilar arteries.Results The scores of the neurobehavior significantly decreased in the 3 d,5 d,7 d and 14 d in operation group(8.33±0.38,6.67±0.20,4.83±0.31,9.33±0.51,respectively) and showed significant difference compared with the control and sham group (P＜0.01).There was statistically significance between the different time points(P＜0.01).The scores of treatment group were 10.00±0.65,10.17±0.66,9.83±0.61,10.67±0.70 respectively and the difference was statistical significance(P＜0.01) compared with the operation group.The expression of the Cx43 protein increased in the 1 d,3 d,5 d,7 d and 14 d after operation which were (0.289±0.01)％,(0.389±0.008)％,(0.51±0.006)％,(0.651± 0.019) ％,(0.329±0.151)％,respectively and had statistical significance (P＜0.01) compared with the control and sham group.There were statistical significance among the different time points (P＜0.01).The expression were (0.225±0.007) ％,(0.228±0.01) ％,(0.251 ±0.02) ％,(0.303±0.008) ％,(0.267±0.008) ％ in the I st,3rd,5th,7th,and14th day after treatment and had statistical significance compared with the control and sham group(P＜ 0.01).The eonductivities were (3.07±0.19) nS/m,(4.88±0.34) nS/m,(8.20±0.31) nS/m,(11.94±0.22) nS/m,(4.07±0.22) nS/m,respectively,and had important increment in the 1 st,3rd,5th,7th and 14th day after operation compared with the control and sham operation group (P＜0.01).There were statistically significance in the different time points(P＜0.0l).And the data of the treatment group were (1.38±0.16) nS/m,(1.64±0.15)nS/m,(2.26± 0.21) nS/m,(2.89±0.85) nS/m,(2.11±0.20) nS/m respectively and had statistical significance compared with the operation group(P＜0.01).Conclusions Cx43 proteins play an important role in the pathomechanism of cerebral vasospasm after experimental subarachnoid hemorrhage.Gap junction inhibitor 18β-glycyrrhetinic-acid can relieve cerebral vasospasm after experimental subarachnoid hemorrhage in rats in vivo.