Function and quality of life results after ileal pouch surgery for chronic ulcerative colitis and familial polyposis.

The aim of this study was to assess gastrointestinal function and quality of life, including occupational, social, and sexual function, in 75 patients who underwent pelvic pouch construction between November 1984 and May 1988 at our institution. Complications occurred in 45 percent of patients after pouch construction and in 17 percent after ileostomy closure. One patient died from sepsis caused by an anastomotic leak after ileostomy closure. The most common complication was a pouch-anal anastomotic stricture (22 percent), and the complication with the greatest potential morbidity was pouch-anal dehiscence (8 percent), which was highly predictive of pouch failure. Functional results were assessed by questionnaire during the 3-month period after ileostomy closure in all 58 patients who successfully attained intestinal continuity. A second assessment was performed at 15 +/- 11 months after ileostomy closure in 52 patients whose continuity had been restored for longer than 3 months. In an overall assessment, 94 percent of all patients with restored intestinal continuity (73 percent of entire patient group) rated the pouch as being superior to a permanent ileostomy and 92 percent (71 percent of entire group) would go through another pouch procedure. These results support the continued recommendation of this procedure as an acceptable alternative to proctocolectomy and permanent ileostomy in patients with ulcerative colitis or familial polyposis.

Investigations of the anal sphincter before and after restorative proctocolectomy.

Twenty-eight patients who underwent sphincter-saving proctocolectomy and formation of an ileoanal reservoir had clinical evaluation of resting and maximal anal sphincter pressures and perfused catheter manometry. The clinical estimate of resting tone, heretofore believe to be a good predictive parameter of postoperative function, was inaccurate. This suggests the advisability of manometric evaluation. There were significant changes in sphincter pressures postoperatively. Operation did not effect the preoperative electromyographic findings of the puborectalis muscle and external sphincter in our small postoperative population. The mechanism by which operation might influence these parameters has been discussed. Factors such as parity and the descending perineum syndrome may effect continence. Due to the length of time the sphincter is required to function in these patients and the multiplicity of factors involved, we believe that long-term studies are needed.

Effects of monoclonal antibodies to somatostatin on somatostatin-induced and intestinal fat-induced inhibition of gastric acid secretion in the rat.

Cell lines producing monoclonal antibodies to somatostatin, designated S10 and S20, have recently been generated. The purpose of the present immunoneutralization study was to examine the ability of these antibodies to block the inhibitory effect of exogenous somatostatin on meal-stimulated gastric acid secretion in the innervated rat stomach and to use these antibodies as probes to determine if somatostatin is involved in intestinal fat-induced inhibition of gastric acid secretion. The plateau acid secretory response to a liver extract meal in this model was 28 +/- 2 mu Eq/30 min. Intravenous infusion of somatostatin at 2.0 micrograms/kg X h or intraduodenal oleic acid at 1.2 ml/h reduced this response to 12 +/- 1 and 14 +/- 1 mu Eq/30 min, respectively. The antibodies were given intravenously 1 h before the meal and either somatostatin or intraduodenal oleic acid infusion. S10 preinfusion returned the plateau meal responses to the levels seen with the meal alone: 25 +/- 4 and 26 +/- 1 mu Eq/30 min, respectively. S20 preinfusion had no effect, the responses being 14 +/- 1 and 16 +/- 1 mu Eq/30 min, respectively. These results demonstrate successful binding of exogenous somatostatin by S10 in vivo and reversal of intestinal fat-induced inhibition of gastric acid secretion by S10 preinfusion. It is concluded that the mechanism whereby fat in the small intestine inhibits gastric acid secretion may involve the release of somatostatin.

Increased antral G-cell number and gastrin content in dogs after massive small bowel resection.

The effects of massive small-bowel resection on antral gastrin tissue concentration and G-cell number have been investigated in the dog. Tissue gastrin concentrations increased significantly after resection from 16.8 +/- 2.6 ng/mg wet weight to 30.3 +/- 3.2 ng. Immunoreactive gastrin cell number also increased from 29.8 +/- 2.5 cell/mm2 to 43.1 +/- 3.0 cells/mm2. Immunocytochemistry demonstrated that the hyperplastic gastrin cells were found in small groups, with the majority of the immunoreactivity located at the luminal pole of the cells. This finding, linked to hypogastrinemia in the dogs after massive small bowel resection, suggests that some of the hyperplastic G cells may have an exocrine rather than endocrine function.

Evidence for vagus-dependent pancreatic polypeptide-releasing factor in the antrum: studies with the autotransplanted dog pancreas.

Pancreatic polypeptide (PP) response to food is suppressed by truncal vagotomy, antral vagotomy, and antrectomy. The inhibitory effect of antral vagotomy and of antrectomy may be due to inadvertent vagal denervation of the pancreas, disruption of antropyloric neural reflexes, or inhibition of release of a PP-releasing factor from the antrum. In this study we examined the latter hypothesis by achieving total extrinsic pancreatic denervation by orthotopic autotransplantation of the entire pancreas in four dogs. Total extrinsic pancreatic denervation, which abolished the pancreatic juice protein response to insulin, did not significantly alter plasma PP response to a meal (peak 30-minute PP of 696 +/- 192 pg/ml before transplantation versus 961 +/- 80 pg/ml after transplantation). Therefore, postprandial release of PP is, to a large extent, not mediated either by direct vagal innervation of the pancreas or by neural communications between the pancreas and antrum or the pancreas and the small intestine. In two of the dogs with pancreatic transplants, subsequent antral vagotomy resulted in greater than 80% inhibition of postprandial PP response. These findings are consistent with the hypothesis that a PP-releasing factor is present in the antrum and that the release of this factor is dependent on intact antral vagal innervation.

Gastric and pancreatic hyposecretion following massive small-bowel resection.

It is well established that massive small-bowel resection (MSBR) invariably causes hypersecretion of acid in animals with denervated gastric pouches. The effect of MSBR on the secretory responses of both the totally innervated stomach and pancreas have been less well studied. Eighteen adult mongrel dogs were prepared with chronic gastric and pancreatic fistulae. In eight, massive small-bowel resection was performed in addition. Bowel resection did not alter the responses to graded doses of pentagastrin. However, in response to the intragastric titration of a liver extract meal, it had the following effects: (1) profound gastric acid hyposecretion; (2) reduction in pancreatic bicarbonate and protein secretion; and (3) increase in basal and meal-stimulated serum glucagon levels. Hypergastrinemia did not occur after resection. The hyposecretory responses may represent either increased inhibition or decreased secretory stimulation.

Colonic inhibition of gastric acid secretion in the dog.

The colon has been shown to contain an abundance of endocrine cells. Their role is not yet understood. In four dogs prepared with chronic gastric fistula and colonic fistula in the cecum the effects on pentagastrin dose responses of colonic perfusion with the following substance were studied: saline, 15% liver extract pH 7.0; sodium oleate pH 9.4; and 0.08 M HCl. The responses obtained in each of the perfusion studies were compared with those obtained without colonic perfusion. Whereas saline had no effect on these responses, liver extract, sodium oleate, and HCl, each produced significant inhibition. These results suggest that the colon has the capacity for inhibiting gastric acid secretion by some mechanism which may prove to be humoral. Until now the colon has rarely been considered in any assessment of the gut functioning as an endocrine organ. Perhaps a colonic endocrine role should now be given further consideration.