ABSTRACT
AIM To observe the effect of intravenous injection of erythromycin (EM) on interdigestive migrating motor complex (MMC) and postprandial gastrointestinal contraction in conscious dogs , and to study its possible mechanism. METHODS Gastrointestinal contractile activity was recorded using low compliance capillary water perfusion manometric system. EM was administered intravenously during phaseⅠ and after meal, and blood samples were drawn for measuring plasma motilin concentrations. RESULTS ①Plasma motilin levels showed cyclical fluctuations in different phases of MMC, and plasma motilin reached peak during phaseⅢ and lowest during phaseⅠ.②EM induced phaseⅢ-like contractions in the antrum and duodenum, which was not accompanied by a peak in plasma motilin level. The optimum dose of EM for resulting in a premature phaseⅢ with the same characteristics as the spontaneously occurring phaseⅢ was established to be 0.5 mg*kg-1. The dose of 10 mg*kg-1 EM induced gastrointestinal continuous contractions and duodeno-gastric retrograde peristalsis which was associated with retching and vomiting. ③Atropine obviously inhibited EM-induced phaseⅢ activity in the antrum and duodenum. ④EM powerfully enhanced postprandial gastrointestinal contractile activity. CONCLUSIONS The results suggests that EM is a potent prokinetic agent. The mechanism is not related to the release of motilin, but may be mediated partially by cholinergic pathway.
ABSTRACT
AIM To observe the effect of intra- venous injection of erythromycin (EM) on interdigestive migrating motor complex (MMC) and postprandial gastrointestinal contraction in conscious dogs, and to study its possible mechanism. METHODS Gastrointestinal contractile activity was recorded using low compliance capillary water per fusion manometric system. EM was administered intravenously during phase I and after meal, and blood samples were drawn for measuring plasma motilin concentra- tions. RESULTS ①Plasma motilin levels showed cyclical fluctuations in different phases of MMC, and plasma motilin reached peak during phaseⅢ and lowest during phase Ｉ. ②EM induced phase Ⅲ -like contractions in the antrum and duodenum, which was not accompanied by a peak in plasma motilin level. The optimum dose of EM for resulting in a premature phaseⅢ with the same characteristics as the spontaneously occurring phaseⅢ was established to be 0. 5 mg.kg-1. The dose of 10 mg.kg-1 EM induced gas- trointestinal continuous contractions and duodeno-gas-tric retrograde peristalsis which was associated with retching and vomiting. ③Atropine obviously inhibited EM-induced phase Ⅲ activity in the antrum and duodenum. GEM powerfully enhanced postprandial gastrointestinal contractile activity. CONCLUSIONS The results suggests that EM is a potent prokinetic agent. The mechanism is not related to the release of motilin, but may be mediated partially by cholinergic pathway.