You C H, Chey W Y
Gastroenterology. 1984 Jun;86(6):1460-8.
The relationship between electric and mechanical activities of the gastric antrum was investigated in both humans and dogs. In 2 patients, in whom platinum monopolar electrodes were implanted on the serosal surface of the antrum and a perfused manometric tube was placed in the stomach, the number of gastric contractions detected by manometry was only less than 50% of the pacesetter potentials accompanied by action potentials or second potentials. No contraction of the stomach was recorded by manometry when pacesetter potentials occurred without action potentials or second potentials. The relationship was further investigated in 11 anesthetized dogs prepared with implanted electrodes and sensitive ministrain gauges implanted on the serosal surface of the stomach and an intragastric manometric tube. In these dogs, phasic contractions were always recorded by the method using ministrain gauges although the electrical activity showed only PSPs without action potentials or second potentials. The manometry, however, could not recognize these phasic contractions. When the stomach was stimulated by bethanechol infusion through the splenic artery, as in the human stomach, the manometry detected less than 50% of gastric contractions detected by the strain gauge recording. The gastric dysrhythmia including tachygastria, tachyarrhythmia, and bradygastria was induced in 10 dogs by epinephrine, 100 micrograms X kg-1 X h-1, infused via the splenic artery. During the period of gastric dysrhythmia, the phasic contractions disappeared and no contraction associated with action potential could be observed. The phasic contractions reappeared as long as the PSPs occurred regularly in a frequency of 4-5 cycles/min during either the control period or during the period of epinephrine infusion. The epinephrine-induced gastric dysrhythmia was blocked or reversed to normal pacesetter potentials by intraarterial infusion of phentolamine. Our study suggests the following: (1) the pacesetter potentials not only pace and direct gastric contraction, but they may also play a role in the genesis of phasic contractions of the stomach, and (2) gastric contractions detected by sensitive strain gauges are not always recorded by the intraluminal manometry and, thus, gastric dysrhythmia may not be detected by the manometry in humans.
研究了人类和犬胃窦电活动与机械活动之间的关系。在2例患者中，将铂单极电极植入胃窦浆膜表面，并在胃内放置一根灌注测压管，测压法检测到的胃收缩次数仅不到伴有动作电位或二次电位的起搏电位的50%。当起搏电位出现而无动作电位或二次电位时，测压法未记录到胃收缩。在11只麻醉犬身上进一步研究了这种关系，这些犬植入了电极，并在胃浆膜表面植入了灵敏的微型应变计和胃内测压管。在这些犬中，尽管电活动仅显示无动作电位或二次电位的PSP，但使用微型应变计的方法总能记录到阶段性收缩。然而，测压法无法识别这些阶段性收缩。当像在人类胃中一样通过脾动脉注入氨甲酰甲胆碱刺激胃时，测压法检测到的胃收缩不到应变计记录检测到的胃收缩的50%。通过脾动脉以100微克·千克⁻¹·小时⁻¹的速度注入肾上腺素，在10只犬中诱发了包括胃动过速、心律失常和胃缓在内的胃节律紊乱。在胃节律紊乱期间，阶段性收缩消失，未观察到与动作电位相关的收缩。只要在对照期或肾上腺素注入期PSP以4 - 5次/分钟的频率有规律地出现，阶段性收缩就会再次出现。通过动脉内注入酚妥拉明，肾上腺素诱发的胃节律紊乱被阻断或恢复为正常的起搏电位。我们的研究表明：（1）起搏电位不仅为胃收缩设定节律并引导其进行，还可能在胃阶段性收缩的发生中起作用；（2）灵敏的应变计检测到的胃收缩并不总是能被腔内测压法记录到，因此，人类的胃节律紊乱可能无法通过测压法检测到。
