The Effect of Nitric Oxide on Gallbladder Motility

Hong, Soon Chan; Chang, Ki Churl

Abstract

BACKGROUND/AIM: Abnormality in GB motility is related with many gallbladder diseases including GB stone. Gallbladder motility is controlled by both hormonal and neural mechanisms. CCK, gastrin, motilin play a role on gallbladder contraction and VIP, somatostatin are inhibitory agents. Nitric oxide(NO) is known to account for the biologic properties of endothelium dependant relaxing factor. It also plays an important role in mediation of relaxation in various types of non-vascular smooth muscle of GI tract. The objective of this study was to determine the effect of nitric oxide in human gallbladder muscle. METHOD: In this study, nitric oxide was generated by photolysis using long wave-length UV lamp(366 nm) on NO carrying molecule, streptozotocin. GB muscle strips were obtained from 10 cholecystectomized patients and contracted by potassium or CCK-8. We also investigated the effect of methylene blue, which is a inhibitor of guanylate cyclase, after addition of methylene blue to the organ bath containing streptozotocin. Gallbladder movements were recorded using Polygraph(Grass model 79E, USA). And we identified the production of nitric oxide using nitrite assay in our No generating system.
RESULTS
1. Streptozotocin, No containing compound, released NO when UV irradiated. The longer UVR and the higher concentration of STZ, the larger is the amount of produced NO. 2. The human GB muscle was relaxed immediately by photo-induced NO and rapidly disappeared. The maximal relaxation under STZ, 60 sec UVR was 23.1 % comparing potassium or CCK induced contraction. 3. The relaxation was significantly inhibited by methylene blue, the inhibitor of gualylate cyclase.
CONCLUSION
According to above results, we confirmed that nitric oxide relaxed human gallbladder muscle. And we think that the further study should be done to examine whether the L-arginine/NO pathway exist in human GB.