A200 AGA ABSTRACTS

1251

ELECTROACUPUNCTURE MAY RELAX THE CONTRACTIONOF HUMAN SPHINCTER OF ODDI VIA THE CHOLECYSTOKI­NIN RELEASE.Sung-Koo Lee, Myung-Hwan Kim, Hong-Ja Kim, Hyun-Ju Park, Kyo­Sang Yoo, Dong-Wan Seo, Young-II Min, Ji-Hoon Kim, Byung-I1 Min,Asan Med Ctr, Univ of Ulsan Coil of Medicine, Seoul, South Korea; AsanMed Ctr, Seoul, South Korea; Myung-Ji Hosp Kwandong Univ Coil ofMedicne, Seoul, South Korea; Univ of Kyung Hee Coil of Oriental Med­icine, Seoul, South Korea.

Background and aims; There are many factors that effect sphincter of Oddi(SO) motility such as drugs, hormones and neural stimuli. This study wasdesigned to observe the objective effect of electroac upuncture on SOmotility. Methods; Eleven patients (M: F= 5: 6) who had various kinds ?fbiliary disorders were investigated. The conventional ERCP manometncmethods with low-complaint continuously perfused technique were used.After baseline monitoring for phasic wave contractions, electroacupunctureand electrica l stimulation were applied with a mode of 2Hz for 3 msec. Theacupuncture point (GB 34) that has been known to effect biliary system inOriental medicine was selected. We have also stimulated acupomt 5 cmaway from the GB 34 acupoint as a control. During ERCP manometry ,serum cholecystokinin (CCK) levels were measured before, during andafter electroacupuncture. Results; The basal pressure, amplitude and fre­quency of SO contraction were significantly decreased after application ofelectroacupuncture within several minutes. After removal of the acupunc ­ture stimulation, SO motility was restored immediately . Stimulation ofcontrol acupoint, however , did not inhibit the SO contractility. Serumlevels of CCK were significantly increased during e1ectroacupuncture andrestored to basal level after terminat ion of acupuncture . Conclusion ; Elec­troacupuncture of the acupoint GB 34 showed reversible inhibition of theSO contraction. We speculated that the response of the SO to electroacu­puncture may be mediated by some neurohormonal mechanisms includingCCK. Because of the lack of side effects and its simplicity. acupuncturemay be one possible solution for the treatmen t of SO dyskinesia.

1252THE EFFECT OF PHOSPHODIESTERASE INHIBITION ONSPHINCTER OF ODDI MOTILITY: ANOTHER MECHANISM TODECREASE GALLSTONE FORMATION?Brian A. Lindamann, Jeffrey L. Conklin , Joseph J. Cullen , Univ of IowaColi of Med, Iowa City, IA; Univ oflowa Hospitals and Clinics, Iowa City,IA.

Recent evidence suggests that coffee consumption decreases the risk ofsymptomatic cholelithiasis (lAMA 281:2106, 1999). Caff~ine. a phospho­diesterase (POE) inhibitor, may decrease gallstone formation by a numberof mechanisms including increasing bile flow, impairing biliary cholesterolcrystallizatio n, and decreasing gallbladder fluid absorption. AIMS : Todetermine the effect of caffeine and specific POE inhibitors on sphincter ofOddi motility ill vitro. METHODS : Sphincter of Oddi muscle strips fromopossums were attached to force transducers to determine spontane ouscontractions and electrical field stimulation-induced relaxation (BFS). Caf­feine, Vinpocetine (VIN, type I POE inhibitor), Erythro-9-[2-hydroxy-3­nonyl]adenine HCl (EHNA, type II P!JE inhibitor), Zarderverin~ (~~RD,type IIIIIV POE inhibitor), and Zapnnast (ZAP, type V POE inhibitor) ,were added to the tissue baths. RESULTS : Caffeine, ZARD and VINdecreased the frequency and force of spontaneous contractions. (Table :Values are Means:':: SEM, "P < 0.05 vs control.) Caffeine and VINdecreased baseline tone. ZARD increased EFS relaxation while VIN de­creased EFS relaxation. EHNA and ZAP had little effect on in vitrosphincter of Oddi motility. CONCLUSIO NS: Caffeine relaxes the sphinc­ter of Oddi through type I, III, or IV POE pathways. The smoo~h musclerelaxation induced by POE inhibition in the sphincter of Oddi may beanother mechanism that contributes to the decreased incidence of choleli­thiasis with coffee consumption. Support: VA Research Service.

Cycles(bpm) Force of Baseline Tone EFS Relaxationcontraction (glcm') (g) (gtcm2)

Control 4.0±1.0 145±21 1.6±O.2 -28±7Caffeine (10-3) O.8±O.5* 10±1.0* 1.2±O.1* -31±5Control 4.5±1.0 229±46 1.4±O.2 -28±3Zard(1O"') O.2±O.2* O±O* 1.2±O.1 -39±6*Control 3.5±O.7 118±39 1.6±O.2 -35±7VlN (lo-i ) O.1±O.1* 13+13' O.8±O 1' -28+6'

1253ENHANCEMENT OF GALLBLADDER FILLING AND CAER­ULEIN-INDUCED EMPTYING AFTER GLYCERYL TRINITRATEADMINISTRATION IN PATIENTS WITH GALLBLADDER DYS­KINESIA.Laszlo Madacsy, Attila Szepes, Viktoria Bertalan, Mate L~ar, Las~lo

Pavics, Janos Lonovics, First Dept of Med A Szent-Gyorgyi Med Un~v.

Szeged, Hungary ; Dept of Nuclear Med A Szent-Gyorgyi Med Univ,Szeged, Hungary.

Introduction: Acalculous biliary pain (ABP) may be caused by gallbladder(GB) dyskinesia. ABP thought to be elicited by a vigorous contracti le

GASTROENTEROLOGY Vol. 118, No.4

response of the GB neck area at the time of GB contraction evoked byendogenous cholecystokinin that results a functional cy~tic ~uct obstruc­tion and ineffective GB emptying. Although GB dyskinesia due to anuncoordinated GB contraction is an attractive theory, no human data areavailable yet as to provide support for this pathomechanism in patients withABP. Methods: Quantitative hepatobiliary scintigraphy (QHBS) was per­formed in 33 patients with ABP. After overnight fast, 4 lOCi 99mTc­EHIDA was injected iv. Digital images were obtained at one frame/min for120 min. At the 60th min 29 patients with ABP had sufficient GB filling toevoke GB contraction with caerulein (CA) administration, therefore forthese patients I nglbwkglmin CA (Takus, Pharmitalia) was administered ivfor 10 min and the GB ejectio n fraction (GBEF) was determined. 30minutes after the completion of the first contraction an identical dose of CAwas given. At the same time for 22 patients 0.5mg of glyceryl trinitrate(GTN) (Nitromint, EGIS) and for 7 patients placebo was co-administeredsublingually, then the GBEF was calculated repeatedly. In the remaining 4patients without sufficient GB filling at 60th min only GTN was adminis­tered. Results: Hepatic bile secretion and transpapillary bile flow wasnormal in all patients. In 4 patients with no or insufficient GB filling at 60th

min GTN administration caused an abrupt and prominent filling of the GB .In 22 patients the GBEF was significantly increased after GTN and CAco-administration when compared to CA alone, 39.8%+ 24.2% vs.18.9%+ 10.5%, respectively . However in 7 patients placebo caused nosignificant changes in the CA e~oked GBEF , 20.2~+ 1.4.4% .vs.22.2% + 20.6%, respectively. Conclusions: GTN caused a significant Im­provement in both OB filling and emptying in patients with ABP, indicat­ing that impairment of GB function is caused by a functional spasm of thecystic duct rather than organic GB disease . Our results provide the firstdirect evidence that GB dyskinesia i.e. a pure motility disorder may beresponsible for abnormal GB function and subjective complaints of pa­tients with ABP.

1254

MIGRAINE HEADACHES AND SPHINCTER OF ODDI DYS·FUNCTION: IS THERE ANY RELATIONSHIP?William E. Maher, Joseph E. Gcenen, Michael J. Schmalz, Marc F.Catalano, St Luke' s Med Ctr, Milwaukee, WI.

Migraine attacks occur in up to 15% of the population of Western societieswhereas sphincter of Oddi dysfunction occurs less than I %. The mecha­nism of migraine and sphincter of Oddi attacks remain mysterious. Fashioncontinues to swing between neural and vascular theories . However, inmigraine attacks the vascular theory is most widely accepted with transientsmooth muscle contract ions, spasm with the onset of an aura and then localmediators causing vase-vascular dilatation and onset of the throbbingheadache. With sphincter of Oddi dysfunction, the smooth muscle becomesspastic and will have an increased basal pressure recording causing .a~­

dominal pain and possible increase in liver enzymes and acute pancreatitis.AIM: To determine if people with sphincter of Oddi dysfunction have ahigher incidence of migraine attacks than the general population ~nd thusa potential for smooth muscle hypersensitivity. METHOi?S : Sphincter ofOddi dysfunction was defined as a basal pressure recording greater than40mm of mercury. A retrospective study was performed with the identifi­cation of 171 consecutive patients with documented sphincter of Oddidysfunction using a computer database retrieval system. Each pat ient wassent a questionnaire asking if they suffered from frequent migraine attacksand to determine if there was any relationship between abdominal pain andmigraine attacks. RESULTS: One hundred seventy-one questionnaireswere sent out with 90 responses received. Forty-nine/90 (54%)of theresponders stated that they did not have migraine attacks. The remaining41/90 (46%) of the patients with sphincter of Oddi dysfunction reportedfrequent migraine attacks occurring greater than 3-5 times per year . CON­CLUSIO N: Patients with sphincter of Oddi dysfunction have a higherprevalence of migraine attacks than the general population. Th is may be anincidental relationship, however, further investigat ion may be warranted todetermine if smooth muscle hypersensitivity may exist in both migraineattacks and sphincter of Oddi dysfunction.

1255EFFECTS OF FEEDING ON SPHINCTER OF ODDI CYCLIC MO­TILITY IN CONSCIOUS DOGSToshinaga Nabae, Takao Otsuka, Ken Inoue, Shunichi Takahata, KazunoriYokohata, Hirokazu Noshiro, Masao Tanaka, Graduate Sch of Medicine,Kyushu Univ, Fukuoka, Japan .

Background: The Sphincter of Oddi(SO) locates at the junction of thecommon bile duct(CBD) and pancreatic duct and it plays an important rolein bile delivery to the duodenum and prevention of duodenobiliary reflux.During fasting, the SO phasic contractions and basal pressure exhibit acyclic change in coordination with the migrating motor complex (MMC) ofthe gastrointestinal tract. However, the biliary motility after feeding inconscious state has not been investigated well. Methods : Four consciousmongrel dogs with a duodena l cannula underwent a manometric study ofbiliary system, stomach and duodenum during fasting. Basal pressure,amplitude, frequency, motility index of SO phasic waves, common bileduct(CBD) pressure were measured during whole cycle of MMC . After Icycle of MMC, the response of these parameter to feeding( solid meal)during duodenal phase I were also evaluated. Results: (I) The CBDpressure and SO basal pressure gradually decreased from phase II to phaseIII of the duodenal MMC . The SO amplitude gradually increased from