Background: It has been suggested that transient lower esophageal sphincter relaxation is involved in the occurrence of gastroesophageal reflux disease (GERD) and that decreased gastric emptying is an exacerbating factor of transient LES relaxation. In addition, the gastric emptying function is considered to be closely related to gastric motility. Methods: Gastric activity was evaluated by electrogastrography (EGG) in 22 patients with endoscopically positive reflux esophagitis (15 with mild esophagitis of Los Angeles grade A or B and seven with severe esophagitis of Los Angeles grade C or D) and 20 normal individuals. The gastric emptying function was also evaluated by abdominal ultrasonography. The sampling cycle of EGG was 1 s, and the measured frequency was 2.1–6.0 cycle/min (c.p.m.). The mean amplitude of EGG was compared by EGG spectral analysis among brady‐gastria cases with a contraction frequency of less than 2.4 c.p.m., normo‐gastria cases with a contraction frequency of 2.4–3.6 c.p.m., and tachy‐gastria cases with a contraction frequency exceeding 3.6 c.p.m. Results: In the patients with GERD, both the frequency of 3‐c.p.m. waves and peak frequency were reduced, and the gastric emptying function examined by ultrasonography had deteriorated, in comparison with normal individuals. Of those with GERD, the ultrasonographic gastric emptying function was significantly reduced in all patients with severe esophagitis compared with those with mild esophagitis, but the differences of the frequency of 3‐c.p.m. waves, the peak frequency, were not significant. Also, no significant difference was observed in the frequency of 3‐c.p.m. waves or the ultrasonographic gastric emptying function between the 16 patients with hiatal hernia and the six patients with no hiatal hernia. However, the mean amplitude in brady‐gastria and tachy‐gastria was significantly increased in the patients with hiatal hernia compared to those without hiatal hernia. Conclusions: Reduced gastric motility was suggested to be involved in the development of reflux esophagitis, and the presence of hiatal hernia was considered to have some effect on gastric motility.

Nizatidine (CAS 76963-41-2, Acinon), an H2 receptor antagonist, not only inhibits acid secretion but also improves gastrointestinal motility. However, autonomic nervous function has not been studied in detail using electrogastrography (EGG). In the present study, two protocols were adopted to study nizatidine's effects on cardiac autonomic function and gastric motility. Protocol I--Acute: "Group C-I": 10 healthy volunteers received a single oral dose of nizatidine 150 mg. Protocol II--Chronic: "Group DM without N": 15 patients with diabetes mellitus (DM) were observed prior to administration of nizatidine. "Group DM with N": The same 15 patients with DM received nizatidine 300 mg/day for more than 30 days. "Group C-II": This control group was composed of 15 healthy volunteers not receiving nizatidine. In all groups, EGGs were recorded before and after a meal, and autonomic nervous function and QT interval of ECG dispersions were simultaneously evaluated. In Group C-I, nizatidine significantly increased the peak power amplitude of 3 cycles/min (cpm) frequency, but did not significantly change the dominant frequency of the 3-cpm waves. In Group DM with N, nizatidine administration significantly increased the peak power amplitude from 2.4 cpm or a lower frequency (bradygastria) to 3 cpm. Prior to nizatidine administration but after eating a meal, the peak power amplitude on EGG was not increased in Group DM without N. In Group DM with N, however, the EGG peak power amplitude increased to levels similar to those of the healthy subjects (Group C-II). Neither the single nor the chronic administration of nizatidine significantly prolonged the QT interval or increased the QT dispersion. A spectral analysis of heart rate variability showed that nizatidine administration, whether acute or chronic, did not significantly change the indices of autonomic nervous activity. Nizatidine may promote gastric emptying by inhibiting acetylcholine esterase, thus increasing cholinergic activity, and by acting directly on gastric smooth muscle. The results indicate that because nizatidine increases gastric motility without exerting a negative influence on the autonomic nerves, it may be a useful drug in patients with diabetic neuropathy.