Kim C H, Malagelada J R, Azpiroz F, Zinsmeister A R
Dig Dis Sci. 1987 Sep;32(9):1027-32. doi: 10.1007/BF01297194.
The aim of this study was to determine whether food ingestion causes a change in the susceptibility of the stomach to dysrhythmia or in the characteristics of gastric dysrhythmia. The susceptibility of the stomach to develop dysrhythmia was measured by determining the median effective dose of four different drugs known to produce gastric dysrhythmia. These drugs were epinephrine, PGE2, met-enkephalin, and glucagon. The median effective dose for inducing gastric dysrhythmia was measured in four healthy conscious dogs by Dixon's up-and-down method during fasting and after feeding. The median effective dose of epinephrine, PGE2, met-enkephalin, and glucagon were higher after feeding (16.6, 16.6, 35.1, greater than 221 micrograms/kg, respectively) than during fasting (1.7, 5.2, 11.1, 61.0 micrograms/kg, respectively). The results indicate that feeding renders the stomach less susceptible to pharmacologically induced dysrhythmia. However, characteristics of gastric dysrhythmias, such as site of origin and direction of propagation, were similar whether they occurred during fasting or after feeding.
本研究的目的是确定食物摄入是否会导致胃对心律失常的易感性发生变化，或者胃性心律失常的特征是否会发生变化。通过测定四种已知会导致胃性心律失常的不同药物的半数有效剂量，来衡量胃发生心律失常的易感性。这些药物分别是肾上腺素、前列腺素E2、甲硫氨酸脑啡肽和胰高血糖素。在禁食期间和进食后，采用狄克逊上下法在四只健康清醒的狗身上测定诱发胃性心律失常的半数有效剂量。进食后，肾上腺素、前列腺素E2、甲硫氨酸脑啡肽和胰高血糖素的半数有效剂量（分别为16.6、16.6、35.1、大于221微克/千克）高于禁食期间（分别为1.7、5.2、11.1、61.0微克/千克）。结果表明，进食使胃对药物诱发的心律失常的易感性降低。然而，胃性心律失常的特征，如起源部位和传播方向，无论在禁食期间还是进食后发生，都相似。
