Exogenous nitrergic pathway involved in the regulation of gastric myoelectrical activity in dogs.

OBJECTIVE

Although the effect of nitric oxide (NO) on gastric motility has been investigated in numerous studies, its effects on gastric slow waves and spike activity which regulate gastric motility remained largely unknown. The aim of this study was to test the hypothesis that NO would impair gastric slow waves by reducing their regularity and amplitude as well as contraction-related spike activity.

MATERIAL AND METHODS

The study required four sessions in 8 dogs, 2 weeks after the implantation of four pairs of electrodes along the greater curvature of the stomach. In each session, saline, L-arginine (L-Arg) (75 mg/kg), NG-nitro-L-arginine methyl ester (L-NAME) (5 mg/kg) or L-Arg + L-NAME was given intravenously (IV) after a 30-min baseline recording in the fasting state. A solid test meal (200 g) was ingested 30 min after the IV injection of one of the medications. Gastric myoelectrical activity was recorded for 30 min at baseline, 30 min after the IV injection and 60 min after the meal.

RESULTS

The frequency, amplitude and rhythmicity of gastric slow waves were not affected by NO. L-NAME significantly increased spike activity in the fasting state but not in the fed state. L-Arg did not reduce the number of spike bursts per minute (NSPM) in the fed state. Postprandially, there was a significant decrease in slow wave frequency but a substantial increase in the strength and frequency of spike activity.

CONCLUSIONS

Exogenous NO has no effect on the frequency, amplitude or regularity of gastric slow waves; inhibition of NO increases spike activity in the fasting state but not in the fed state.