中文摘要：

目的 探讨Cx43在内皮素诱导的脑基底动脉收缩中的表达变化及其可能的作用.方法 血管环张力实验检测内皮素诱导的脑基底动脉的收缩变化并应用Western blot检测基底动脉Cx43蛋白的表达变化,染料传输实验用来检测脑基底动脉收缩过程中平滑肌细胞间缝隙连接的功能变化.结果 浓度递增的内皮素导致脑基底动脉呈显著浓度依赖性的收缩,一定浓度缝隙连接阻断剂苷珀酸显著缓解该收缩；收缩过程中,Cx43的蛋白表达呈显著时间依赖性的升高,苷珀酸减弱该表达的升高；内皮素刺激下,血管平滑肌细胞间的染料传输呈时间依赖性的升高,苷珀酸显著减少染料在细胞间的传输.结论 脑血管痉挛过程中,通过增加Cx43的表达,血管细胞间缝隙连接的功能被内皮素激活并在血管痉挛病理过程中发挥重要作用；抑制缝隙连接的功能是有效缓解蛛网膜下腔出血后脑血管痉挛的新途径. 关

英文摘要：

Objective To investigate the role of connexin43 in ET - 1 - induced contraction in rabbit basilar artery. Methods The ET - 1 - induced contraction without or with carbenoxolone was studied with an isometric tension system, The expression of connexin43 protein in ET - 1 stimulated basilar arteries was studied with Western blot. Scrape/scratch method was used to analyze the function of gap junction in cultured rabbit cerebrovascular smooth muscle cells. Results ET - 1 produced a concentration - dependent contraction. Carbenoxolone inhibited ET - 1 induced contractiorL The connexin43 protein level was increased in ET - 1 stimulated basilar arteries. Carbenoxolone decreased the connexin43 protein level increased by ET - 1. Cells treated with ET - 1 appeared positive communication and the dye transfer was increased in a time - dependent fashion. Carbenoxolone suppressed the ET - 1 - induced increasement of dye transfer. Conclusions The enhancement of gap junction intercellular communication is activated by ET - 1 via modulating the expression of connexin43, and plays an important role in the pathogenesis of cerebral vasospasm Inhibition of vascular GJIC as a means of reducing cerebral vasospasm after SAH may have therapeutic advantage.