Study of electromechanical activity of the stomach in humans and in dogs with particular attention to tachygastria.

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.