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        전침 자극에 의한 오디 괄약근 운동성 변화에 관한 연구

        이성구(Sung Koo Lee),김명환(Myung Hwan Kim),김홍자(Hong Ja Kim),서동완(Dong Wan Seo),이상수(Sang Soo Lee),김동일(Dong Il Kim),유교상(Kyo Sang Yoo),주연호(Yun Ho Joo),민영일(Young Il Min),김지훈(Ji Hoon Kim),민병일(Byung II Min) 대한소화기기능성질환·운동학회 2000 Journal of Neurogastroenterology and Motility (JNM Vol.6 No.1

        N/A Background/Aims: This study was designed to evaluate the effects of electroacupuncture on the sphincter of Oddi (SO) motility in humans and to correlate the manometric findings with plasma cholecystokinin (CCK) levels. Methods: Eleven patients (M: F= 5: 6) who had various kinds of biliary disorders were enrolled. SO motility was monitored with a conventional low-compliant continously perfused technique using ERCP (n=9) or percutaneous transhepatic cholangioscope (n 2). After baseline monitoring for phasic wave contractions of SO, electroacupuncture was applied at a specific acupoint, GB 34, in these 11 patient.. A nonspecific acupoint 5 cm away from GB 34 was selected as a control. Manometric parameters of SO were also checked in 6 subjects during stimulation of the control acupoint. CCK plasma levels were measured during the time course of electroacupuncture stimulation, Results: All the manometric parameters including the basa1 pressure of SO, amplitude, frequency and duration of phasic wave contraction of SO were significantly decreased (p< 0.05) during electroacupuncture stimu1ation. The inhibition of SO contractility was accompanied by increased CCK plasma levels. After removal of electroacupuncture stimulation, restoration of amplitude and duration to basal condition were noted. A tendency towards the return of SO contractility was also observed in basal pressure and frequency. Stimulation of the control acupoint, however, did not affect the SO contractility and plasma CCK levels. Conclusions: Electroacupuncture stimulation of acupoint GB 34 showed reversible inhibition of SO contraction in humans. We speculate that the response of SO to electroacupuncture stimulation may be mediated by some neurohormonal mechanisms including CCK release. (Korean Journal of Gastrointestinal Motility 2000;6:44-5l)

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