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目的探讨缝隙连接在输尿管痉挛中的作用及其机制。方法新西兰大白兔按随机数字表法分为正常对照组(10只)和实验组(14只)。实验组制作输尿管梗阻模型。常规HE染色、电镜观察输尿管结构变化,采用Western blot及免疫组织化学技术分别检测输尿管中缝隙连接蛋白Cx43的表达变化,以体外肌条拉力实验检测输尿管收缩性变化,并观察缝隙连接阻滞剂18α-次甘草酸(AGA)对其收缩性的影响。结果两组输尿管形态改变差别不明显。输尿管平滑肌细胞间存在大量缝隙连接结构。免疫组化技术及Western blot检测可见实验组输尿管Cx43表达较对照组增加(P<0.01)。体外肌条拉力实验显示实验组在较小电刺激强度[(0.42±0.14)mV]下即可出现自发性收缩(P<0.05);随电刺激强度增大,肌条收缩力逐渐增强,相同电刺激强度下实验组收缩力较对照组明显增高(P<0.05),AGA可显著抑制电刺激所引起的输尿管收缩,而实验组较对照组收缩力下降更为明显(P<0.05)。结论 Cx43介导胞间通讯增强是导致输尿管急性梗阻后兴奋性增高、收缩力增加的重要因素之一。
Objective To explore the role of gap junction in ureteral spasm and its mechanism. Methods New Zealand white rabbits were divided into normal control group (n = 10) and experimental group (n = 14) by random number table. Experimental group ureter obstruction model. The changes of ureteral structure were observed by HE staining and electron microscopy. The expression of connexin Cx43 in ureter was detected by Western blot and immunohistochemistry. The contractility of ureter was measured by in vitro tensile test and the effects of gap junction blockade 18α Effect of Glycyrrhizin (AGA) on Contractility. Results There was no significant difference in ureteral morphology between the two groups. There are a large number of gap junctional structure between ureteral smooth muscle cells. Immunohistochemistry and Western blot showed that the ureteral Cx43 expression in the experimental group increased compared with the control group (P <0.01). In vitro muscle tension test showed that spontaneous contraction (P <0.05) could be observed in the experimental group with small electrical stimulation intensity [(0.42 ± 0.14) mV]; contractility of the muscle strips gradually increased with the increase of electrical stimulation intensity The contractile force of the experimental group was significantly higher than that of the control group (P <0.05). The AGA significantly inhibited the ureteral contraction induced by electrical stimulation, but the contractility of the experimental group was significantly lower than that of the control group (P <0.05). Conclusion Cx43-mediated enhancement of intercellular communication is one of the important factors that lead to increased excitability and contractility after acute ureteral obstruction.