BACKGROUND: This study was designed to evaluate the effects of electroacupuncture on sphincter of Oddi (SO) motility in humans and to associate the manometric findings with cholecystokinin (CCK) plasma levels. METHODS: Eleven patients (M:F = 5:6) with various kinds of biliary disorders were enrolled. SO motility was monitored with conventional low-compliance, continuous perfusion technique at ERCP (n = 9) or via percutaneous transhepatic cholangioscopy (n = 2). After baseline monitoring for phasic wave contractions of SO, electroacupuncture was applied at a specific acupoint GB 34. A nonspecific acupoint 5 cm away from GB 34 was selected as a control. Manometric parameters of the SO were also measured in 6 subjects during stimulation of the control acupoint. CCK plasma levels were measured during electroacupuncture stimulation. RESULTS: All manometric parameters including basal pressure, amplitude, frequency, and duration of phasic wave contractions of the SO were significantly decreased (p < 0.05) during electroacupuncture stimulation. The inhibition of SO contractility was accompanied by increased CCK plasma levels. After discontinuation of electroacupuncture stimulation, restoration of amplitude and duration to basal conditions was noted. A tendency toward return of SO basal pressure and contractile frequency to baseline was also observed. Stimulation of the control acupoint did not affect SO contractility. CONCLUSION: Electroacupuncture stimulation of acupoint GB 34 resulted in reversible inhibition of SO contraction in humans. The response of SO to electroacupuncture stimulation may be mediated by some neurohormonal mechanisms including CCK release.
BACKGROUND: This study was designed to evaluate the effects of electroacupuncture on sphincter of Oddi (SO) motility in humans and to associate the manometric findings with cholecystokinin (CCK) plasma levels. METHODS: Eleven patients (M:F = 5:6) with various kinds of biliary disorders were enrolled. SO motility was monitored with conventional low-compliance, continuous perfusion technique at ERCP (n = 9) or via percutaneous transhepatic cholangioscopy (n = 2). After baseline monitoring for phasic wave contractions of SO, electroacupuncture was applied at a specific acupoint GB 34. A nonspecific acupoint 5 cm away from GB 34 was selected as a control. Manometric parameters of the SO were also measured in 6 subjects during stimulation of the control acupoint. CCK plasma levels were measured during electroacupuncture stimulation. RESULTS: All manometric parameters including basal pressure, amplitude, frequency, and duration of phasic wave contractions of the SO were significantly decreased (p < 0.05) during electroacupuncture stimulation. The inhibition of SO contractility was accompanied by increased CCK plasma levels. After discontinuation of electroacupuncture stimulation, restoration of amplitude and duration to basal conditions was noted. A tendency toward return of SO basal pressure and contractile frequency to baseline was also observed. Stimulation of the control acupoint did not affect SO contractility. CONCLUSION: Electroacupuncture stimulation of acupoint GB 34 resulted in reversible inhibition of SO contraction in humans. The response of SO to electroacupuncture stimulation may be mediated by some neurohormonal mechanisms including CCK release.