Contribution of Ca influx from extracellular pool and Ca-release from store sites in caffeine-induced contraction of rat portal vein longitudinal muscle were examined. At 37°C caffeine induced a phasic contraction and the contraction was inhibited by verapamil or in the absence of Ca. Under low temperature, it was not decreased remarkably by verapamil or by the removal of extracellular Ca. Na-removal potentiated caffeine-induced contraction in the absence of Ca. Caffeine-induced contraction was also potentiated by high-Kdepolarization. These contractions were at both temperature inhibited greatly by ryanodine. Caffeine induced the burst of the action potential at 37°C but it was not remarkable at 17°C. These results indicate that both extracellular Ca influx and release of stored Ca are involved in the caffeine-induced contraction. However, dependence of the contraction on Ca sources are influenced by temperature, extracellular Na and membrane potential.

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FOY induced a dose-dependent inhibitory response on the gallbladder, sphincter of Oddi and duodenum of normal and gastrectomized dogs, although it induced an excitatory response in some dogs. The inhibitory response was not reduced or terminated by pretreatment with atropine, guanethidine, hexamethonium or/and proglumide. The FOY-induced inhibitory response reversed to the excitatory response in the sphincter of Oddi and duodenum by pretreatment with tetrodotoxin, but not in the gallbladder. These results suggested that the FOY-induced inhibitory response of the sphincter of Oddi and duodenum was caused by stimulation of nonadrenegic noncholinergic inhibitory neurons, not by FOY-induced chole cystokinin secretion. The excitatory response was induced by direct stimulation of their smooth muscles. The inhibitory response of the gallbladder to FOY was induced by direct stimulation of the smooth muscles.

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In a clinical study, we examined the clinical assessment of bowel function and lactulose hydrogen breath test in 14 patients after total colectomy. All patients within one year after ileostomy closure had ‘poor’ function and showed no increase of hydrogen breath gas concentration. 10 of 12 patients more than one year showed increase of hydrogen breath gas concentration, and 8 of them had ‘fair’ function. The oro-neorectal transit time (ONTT) in ‘poor’ group was shorter than in ‘fair’ group and control (p<0.05). The increase of hydrogen breath gas suggests changes of bacterial flora and colonization of the remained ileum.
In an experimental study, we performed subtotal colectomy with the J-pouch reservoir in 11 dogs. We examined ONTT with barium method, gastric emptying with acetaminophen method, and gastrointestinal motility with strain gauge force transducers. Although ONTT at one month after operation had been shorter than control, ONTT at 3 and 6 months became longer than at one month. The gastric emptying after subtotal colectomy was significantly slower than control. Although the propagation velocity of interdigestive migrating complex (IMC) in the jejunum and ileum at 2 weeks had been faster than control, the velocity at 4 weeks and 3 months became slower than at 2 weeks. The frequency of IMC and prolonged propagated contraction in the J-pouch reservoir decreased. The specimen of J-pouch reservoir resected at 6 months showed villous atrophy, crypt elongation, decrease of muscle layers thickness and disappearance of solitary follicles. Therefore, the suppressed motility in each sites of the gastrointestinal tract, increase of anaerobic and colonization of the ileum implied ‘adaptation’ after total colectomy.

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