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Biomedical subjects

H T Debas

Publications and source records attributed to H T Debas.

At least 109 records · Page 6Linked to original sources
PubMed1983

Measurement of prostaglandin E2 in interstitial fluid from the dog stomach after feeding and indomethacin.

The purpose of the study was to develop a method for collecting interstitial fluid bathing the stomach tissues in which prostaglandins could be measured. Hollow dialysis fibers attached at the ends to Silastic tubes were surgically implanted into the submucosa of the gastric fundus and antrum of dogs. The Silastic tubes were exteriorized through the body wall. After full recovery from surgery, the fibers were filled with 5% bovine serum albumin in isotonic saline that was replaced at 5-min intervals. Prostaglandin E2 was measured in the dialysate by radioimmunoassay. In 6 dogs, feeding significantly stimulated the release of prostaglandin E2 into the fundic interstitial fluid from 5.3 +/- 0.6 ng X ml-1 to 12.1 +/- 1.6 ng X ml-1 (p less than 0.01) but had no effect on antral levels. In 4 dogs, indomethacin (0.01, 0.1, 1.0, and 10.0 ng X kg-1, i.v.) caused a dose-dependent depression in prostaglandin E2 levels in interstitial fluid of the fundus and antrum. In 4 other dogs, indomethacin depressed the ex vivo generation of prostaglandin E2 in biopsy specimens of the fundus and antrum. These results validate the technique of interstitial fluid dialysis and suggest that it is a powerful method for examining the secretion of locally acting substances in the stomach of conscious animals.

Animal Feed↗
PubMed1982

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.

Animals↗
PubMed1982

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.

Animals↗
PubMed1981

Neurohumoral inhibitory mechanism initiated by antral distension.

This study examines the effect of graded antral distension with acid (0.1 M HCl) or alkali (0.1 M NaHCO3) on pentagastrin-stimulated acid secretion in two groups of dogs. Group A consisted of six dogs provided with innervated antral pouch. In these dogs, the vagal branches to the fundus, as well as the extragastric vagal divisions (hepatic and celiac), were preserved. All of these animals had a gastric fistula in the main stomach, and in two a denervated fundic pouch or Heidenhain pouch was constructed in addition. Group B consisted of four dogs with an innervated antral pouch and gastric fistula. In this latter group, however, parietal cell vagotomy as well as extragastric vagotomy (division of the hepatic and celiac branches) was performed so that the only vagal communication was between the antrum and the CNS. Antral distension with acid caused significant inhibition of pentagastrin-stimulated acid secretion from both the gastric fistula and the Heidenhain pouch in Group A dogs. Antral acidification without distension did not inhibit. Alkaline antral distension in this group caused much less inhibition of acid secretion, but did cause significant increase in circulating immunoreactive gastrin. In Group B dogs, antral distension with neither acid nor alkali caused inhibition of pentagastrin-stimulated acid secretion, indicating that intact vagal supply to the oxyntic mucosa and/or to the extragastric abdominal organs is necessary for the inhibitory mechanism to operate. The results of this study suggest that: a) antral acidification per se does not inhibit pentagastrin-stimulated acid secretion; and b) antral distension with acid, and to a lesser extent with alkali, is inhibitory only if vagal innervation to the fundus and other abdominal viscera is preserved. The observations are compatible with the hypothesis that antral distension activates a neurohumoral inhibitory mechanism releasing the inhibitor reflexly from sites other than the antrum or CNS.

Animals↗
PubMed1981

Peptic ulcer: new therapies, new diseases.

Although hospitalizations and deaths attributable to peptic ulcer have decreased notably during the past decade, it is not certain whether this decrease is because of reduced incidence of new cases or changes in other factors, such as the severity of the disease. Several genetic traits associated with peptic ulcer have been recognized. Hyperpepsinogenemia I is the most prevalent. Peptic ulcer is a heterogeneous group of disorders with multiple genetic and environmental causes. One manifestation of the diversity of ulcer disease is the variety of physiologic abnormalities seen in patients. The use of endoscopy has enabled more reliable evaluation of new treatments. Histamine H2-receptor antagonists are the dominant mode of treatment, but increasing attention is being given to agents that enhance the resistance of the mucosa to injury, such as prostaglandins. Because of the lower frequency of side effects, proximal gastric vagotomy is gradually replacing truncal vagotomy with drainage. The possibility that endoscopic treatments, such as laser coagulation, may reduce mortality from bleeding ulcers is being investigated.

Duodenal Ulcer↗
PubMed1980

Assessment of the amylase--creatinine clearance ratio in postoperative patients.

The value of the amylase--creatinine clearance ratio (ACCR) in the diagnosis of postoperative pancreatitis was prospectively assessed. In 77 patients undergoing operations known to have a significant incidence of postoperative pancreatitis (gastric, biliary or pancreatic) i.e. "high risk" group, the ACCR was abnormally elevated postoperatively in 36 patients (47%). However, overt clinical pancreatitis occurred in only eight patients (10%). In 60 other patients undergoing nonabdominal operations (orthiipedic, head and neck, varicose vein surgery etc.) i.e. "low risk" group, the ACCR was abnormally elevated postoperatively in 23 patients (38%). No patient in this group developed clinical pancreatitis. We conclude, therefore, the ACCR is often abnormally elevated nonspecifically following any type of surgery, and cannot be used as evidence of postoperative pancreatitis. These data do suggest, however, that a normal ACCR, especially on successive daily determinations, might help to exclude the diagnosis of postoperative pancreatitis.

Acute Disease↗
PubMed1980

Glucagon therapy in acute pancreatitis: prospective randomized double-blind study.

The known suppressive actions of glucagon on the secretion of pancreatic enzymes and of gastric acid, and the reported effectiveness of glucagon in treating acute pancreatitis, prompted the authors to carry out a prospective, randomized, double-blind, controlled trial of this hormone. Sixty-six patients with acute pancreatitis admitted to the surgical service of the Vancouver General Hospital were randomized into two groups of 33, receiving either glucagon or placebo in addition to their conventional therapy. The two groups were comparable with respect to the cause of the pancreatitis and the severity of the disease. Glucagon did not reduce the patients' analgesic requirements or the duration of abdominal signs, ileus, hyperamylasemia or hospital stay. Of the 66 patients, 4 died. Three of these were in the group receiving glucagon. The authors conclude that, contrary to theoretical expectations and the results of past uncontrolled trials, glucagon has no beneficial effect on the clinical course or outcome of acute pancreatitis, irrespective of the etiology or severity of the disease.

Acute Disease↗
PubMed1980

Gastric inhibitory polypeptide (GIP) is not the primary mediator of the enterogastrone action of fat in the dog.

We compared the inhibition of food-stimulated gastric acid secretion and changes in serum concentrations of immunoreactive gastric inhibitory polypeptide and gastrin caused by: (a) duodenal perfusion of oleic acid, and (b) intravenous infusion of pure, natural, porcine gastric inhibitory, polypeptide in dogs with gastric fistula and pancreatic fistula. A rate of duodenal perfusion of oleic acid (12 ml/hr) which gave near maximal pancreatic protein response was chosen. This dose of oleic acid caused complete suppression of acid response to a meal of liver extract (300 ml of a 15% solution) while elevating serum immunoreactive gastric inhibitory polypeptide modestly. By contrast, intravenous administration of gastric inhibitory polypeptide that raised serum immunoreactive gastric inhibitory polypeptide several fold caused only 40% inhibition of acid response to the same meal. Other effects of duodenal perfusion of oleic acid were exaggeration of pancreatic protein secretion and significant inhibition of gastrin release in response to the meal. Exogenous administration of gastric inhibitory polypeptide, on the other hand, was without significant effect on these responses. These results suggest that, in the innervated dog stomach, the enterogastrone action of fat is not primarily mediated by gastric inhibitory polypeptide.

Animals↗
PubMed1980

Physiopathology of lower esophageal diverticulum and its implications for treatment.

This study attempted to define the esophageal motor disturbances and pathogenesis of symptoms in patients with lower esophageal diverticulum. Sixty-five patients were investigated by manometry in addition to roentgenography and endoscopy. Fifty had manometric evidence of abnormal motility, most often diffuse spasm or achalasia. Of the 15 patients with normal esophageal motility, 13 had hiatal hernia, and five of these had a high grade distal esophageal stricture. Pressures in the lower esophagus and lower esophageal sphincter in patients with lower esophageal diverticulum and motor disturbance were the same as for those in matched patients with motor disturbances but no diverticulum. Dysphagia, chest pain and regurgitation were common presenting symptoms. Of 46 patients with dysphagia, only ten had mechanical obstruction to explain this symptom. Of 32 patients with chest pain, only two had ulceration in the diverticulum as a possible cause of pain. We conclude that the development of lower esophageal diverticulum and its symptoms are associated with a motor disturbance of the esophagus in the majority of patients and with an organic obstruction in the minority of patients. The diverticulum itself is usually not the sole cause of the esophageal symptoms, although diverticula can produce symptoms in the absence of other definable conditions. When surgical treatment is indicated, the diverticulum should be excised and the underlying motor or mechanical obstruction should be corrected to prevent serious postoperative complications and recurrence of the diverticulum and its symptoms.

Adult↗
PubMed1980

Functioning heterotopic oxyntic mucosa in the rectum.

Heterotopic gastric mucosa in the rectum is an extremely rare condition. It is significant clinically because it may cause rectal bleeding or may present as a mass which must be distinguished from a neoplasm. Another case is described, and the 9 previously reported cases are reviewed. This is the first case to be reported in which the heterotopic mucosa was actually shown to secrete measurable acid in response to pentagastrin. The lesion could be accurately demarcated using a pH-probe after pentagastrin stimulation, a maneuver which was helpful in the complete surgical excision of the lesion.

Adult↗
PubMed1980

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.

Animals↗
PubMed1980

Fundic inhibition of acid secretion and gastrin release in the dog.

In dogs provided with Heidenhain pouch and gastric fistula, we studied the effect of near-total excision of the fundic mucosa of the main stomach on acid secretion and gastrin release. Fundic mucosal excision abolished the mean response of the gastric fistula and reduced its maximal response to pentagastrin and to histamine by 85%. The basal Heidenhain pouch acid output increased ninefold, and fasting levels of serum gastrin increased from 36 +/- 3 pg/ml before the 248 +/- 47 pg/ml after fundic mucosa excision. The peak gastrin response to meal rose from 168 +/- 12 before to 392 +/- 49 pg/ml after. This increase could not have been due to changes in pH during the meal as meal pH was held constant at 5.5 by the method of intragastric titration in both pre- and postexcision studies. Following fundic mucosal excision, the acid response of the Heidenhain pouch to meal and to both submaximal and maximal doses of pentagastrin and histamine increased markedly. The maximal response to the meal increased from 41 +/- 9 before to 167 +/- 43 after, expressed as percent of the preexcision maximal histamine output. The corresponding changes in the maximal responses to pentagastrin respectively before to 124 +/ 26 and 230 +/- 31 after, again expressed as percent of the preexcision maximal histamine output. These observations suggest that fundic mucosal excision removes an inhibitory mechanism of both acid secretion and gastrin release.

Animals↗
PubMed1979

Evidence for a pyloro-cholecystic reflex for gallbladder contraction.

We studied the effect of graded antral distension on gallbladder contraction both when gastrin release was promoted (alkaline distension) and when gastrin release was blocked (acid distension) in five dogs provided with innervated antral pouch, chronic bile fistula and gastric fistula. Graded distension of the antrum caused graded gallbladder contraction as evidenced by bilirubin output even when gastrin release was completely suppressed. This nongastrin mechanism of gallbladder contraction is abolished by parenteral atropine and by transthoracic truncal vagotomy. These observations provide evidence for a cholinergic, pyloro-cholecystic reflex for gallbladder contraction that is dependent on intact long vagal pathways. Similar reflex mechanisms have been shown to be initiated by antral distension and to cause pancreatic enzyme secretion (pyloro-pancreatic reflex) or acid secretion from the oxyntic gland area of the stomach (pyloro-oxyntic reflex). It would appear, therefore, that the antrum plays a central role in the integration of upper gastrointestinal function not only through the hormone gastrin but also through neural reflex mechanisms.

Animals↗