Hypergastrinemia after vagotomy is not associated with decreased gastric somatostatin

Although hypergastrinemia occurs after vagotomy, the mechanisms responsible are not understood. Somatostatin (SRIF) is a peptide that inhibits gastrin release, is present within the gastric fundus and antrum, and is under vagal control. In this study we have investigated the hypothesis that hypergastrinemia is associated with a decrease in gastric SRIF. We examined tissue levels of SRIF in gastric mucosa and muscle wall in rabbits undergoing vagotomy and pyloroplasty compared with sham-operated controls. We also compared the release of SRIF from gastric glands in response to vasoactive intestinal peptide and calcitonin gene-related peptide. Vagotomy resulted in an increase in gastrin compared with controls in both antrum (1062 ± 176 pmol/gm vs 484 ± 48 pmol/gm) and plasma (236 ± 72 pmol/L vs 29 ± 4 pmol/L; p < 0.05). This was accompanied by an increase in the number of gastrin cells (25 ± 4 vs 9 ± 3; p < 0.05). No significant differences were observed in gastric SRIF levels in either the fundus or antrum (p > 0.5). In addition, there were no differences in the release of SRIF from gastric glands of vagotomized animals compared with controls in response to vasoactive intestinal peptide and calcitonin gene-related peptide (p > 0.5). These data suggest that the elevations in plasma and antral gastrin levels after vagotomy are not a result of alterations in gastric SRIF.