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目的观察A型肉毒毒素(BTX-A)对大鼠食管下括约肌离体肌条自发性收缩及乙酰胆碱(ACh)、P物质(SP)引发的收缩增强是否存在抑制作用,并探讨其作用机制。方法剪取食管下括约肌制备肌条并随机分为对照组、BTX-A组、ACh组、ACh+BTX-A组、ACh+阿托品组、SP组、SP+NK1受体拮抗剂(APTL)-SP组、SP+BTX-A组,采用Biolap420E生物机能实验系统记录肌条在不同条件下的收缩变化。结果BTX-A降低食管下括约肌自发性收缩张力及振幅(P<0.05);ACh可增强食管下括约肌收缩张力及振幅(P<0.01),而BTX-A、阿托品均可抑制ACh的增强效应(P<0.01);SP可增强食管下括约肌收缩张力(P<0.01),其增强效应均可被BTX-A、APTL-SP所抑制(P<0.01)。结论 ACh、SP可增强食管下括约肌的收缩能力,而BTX-A可抑制其引发的收缩增强效应。
Objective To investigate whether BTX-A inhibits the spontaneous contractions of isolated myoelectric strips of the lower esophageal sphincter and the contractile enhancement induced by acetylcholine (ACh) and substance P (SP) in rats and its mechanism of action . Methods Muscle strips of lower esophageal sphincter were prepared and divided into control group, BTX-A group, ACh group, ACh + BTX-A group, ACh + atropine group, SP group, SP + NK1 receptor antagonist Group, SP + BTX-A group, Biolap420E bio-functional experimental system was used to record the contraction of muscle strips under different conditions. Results BTX-A decreased the spontaneous contractile tension and amplitude of lower esophageal sphincter (P <0.05). ACh increased contractile tension and amplitude of lower esophageal sphincter (P <0.01), while BTX-A and atropine inhibited the enhancement of ACh P <0.01). SP can enhance the contractile tension of lower esophageal sphincter (P <0.01), and its enhancing effect can be inhibited by BTX-A and APTL-SP (P <0.01). Conclusion ACh and SP can enhance the contractility of lower esophageal sphincter, while BTX-A can inhibit the contractile enhancement induced by it.