Experimental gastric dysrhythmias and its correlation with in vivo gastric muscle contractions

Abstract

Aim: To study the direct correlation between gastric dysrhythmias and in vivo gastric muscle tone.

Methods: Five healthy dogs were implanted with 4 pairs of electrodes along the greater curvature, with a strain gauge (SG) being sutured parallel to the distal electrodes (2 cm above the pylorus). Intravenous vasopressin was given to induce gastric dysrhythmia. The percentage of regular slow waves and SG energy were calculated.

Results: (1) the regularity of gastric myoelectric activity (GMA) was reduced during and after infusion of vasopressin; (2) SG energy was significantly decreased during the infusion of vasopressin; (3) the decrease in SG energy was well correlated with the reduction in GMA regularity; (4) SG energy was negatively correlated with bradygastria and tachygastria.

Conclusion: Vasopressin inhibits gastric contractions and impairs gastric slow waves; gastric dysrhythmias are associated with the reduced antral muscle contractions, and are indicative of antral hypomotility.

Figure 1

Surgical preparations of stomach. Four pairs of temporary electrodes were implanted along the greater curvature at a distance of 4 cm. The most distal pair was 2 cm above the pylorus. A strain gauge was sutured on the serosal wall parallel to the most distal pair of electrodes.

Figure 2

Sample tracings of gastric myoelectric activity recorded from implanted temporary electrodes and gastric contractions from the attached gastric strain gauge. Top 4 channels are gastric myoelectrical activities recorded using serosal electrodes implanted along the greater curvature. The bottom tracing shows gastric contractions measured from a strain gauge implanted in the distal stomach parallel to Channel 4. It was noticed that slow waves propagate from proximal to distal stomach and each gastric slow wave was coupled with a gastric contractile event.

Figure 3

The regularity of gastric myoelectric activity was reduced with and after infusion of vasopressin, and returned somewhat during the last 20-min recovery period. ANOVA, ^bP < 0.001 baseline vs 2nd or 3rd 20-min period (n = 7).

Figure 4

Distribution of gastric dysrhythmias induced by intravenous infusion of vasopressin. Similar percentage of tachygastria and bradygastria was observed, which contributed to the irregularity of gastric myoelectric activity. ANOVA, ^aP < 0.05 vs baseline and 3rd 20-min period (n = 7).

Figure 5

Illustration of gastric dysrhythmias induced by intravenous Vasopressin. Top 4 channels are gastric myoelectrical activities recorded using serosal electrodes implanted along the greater curvature. The bottom tracing shows gastric contractions measured from a strain gauge implanted in the distal stomach parallel to Channel 4. It was noticed that gastric muscle contractions were absent during periods of tachygastria and bradygastria.