GALLBLADDER CONTRACTION AFTER HORMONAL MANIPULATIONS IN NORMAL SUBJECTS AND PATIENTS UNDER TOTAL PARENTERAL-NUTRITION

Total parenteral nutrition (TPN) induces biliary dilatation, sludge and formation of gallstones. Cholecystokinin (CCK) induces gallbladder (GB) contraction. During thyrotropin-releasing hormone (TRH) testing for thyroid function, we observed that patients felt a strong micturition reflex attributable to smooth muscle contraction of the bladder. The possibility of GB contraction after TRH administration was studied compared to cholecystokinin-octapeptide (CCK-OP) and/or fatty meal administration. The effect of intravenous (IV) CCK-OP), TRH and a combination of the two on GB volume was studied in normal volunteers without GB or liver disease and in patients receiving TPN for > 2 weeks. Subjects included six normal volunteers who received an oral fatty meal only, 18 other normal volunteers (Group A) and 18 TPN patients (Group B). Gallbladder contraction was estimated by ultrasound prior to and after administration of the fatty meal; in the other 36 subjects, GB contraction was calculated prior to and after administration of CCK-OP, TRH, or both. Results are expressed as a percentage of the GB basal volume using each subject as his or her own control. Group A and Group B were each divided into three equal subgroups receiving IV CCK-OP (A1, B1), TRH (A2, B2), or both (A3, B3)Results showed that the fatty meal induced GB contraction by 60%; CCK-OP induced GB volume by 55% in A1 and 50% in B1; TRH induced it by 29% in A2 and 24% in B2; and the combined administration induced GB contraction by 73% in A3 and 69.3% in B3. We concluded that TRH affects GB contraction, and the combination of CCK-OP and TRH is a more potent stimulus of GB contraction than fatty meal alone.