SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Tissue damage from gastric acid may be more prevalent than currently believed following gastric pull-up. An intense anti-acid medical regimen should be instituted peri- and postoperatively. In cases where significant peptic ulcer disease exists preoperatively, an alternative means of reconstruction following laryngo-pharyngo-esophagectomy should be considered.
In chronic gastric fistula rats 0.20 M HCl and 1200 mOsm X kg-1 solution of polyethylene glycol (PEG) infused into a duodenal loop anastomosed to the jejunum (Roux-en-Y) produced maximal inhibition of pentagastrin-stimulated acid secretion, which amounted to 60% and 50%, respectively. In the present study in Roux-en-Y rats with gastric fistula, perfusion of the loop with hyperosmolal (1200 mOsm X kg-1 of PEG solution) 0.20 M HCl produced a greater reduction of the maximal response to pentagastrin (91% inhibition) than perfusion with 0.20 M HCl (64%), suggesting that HCl and hyperosmolal solution inhibit secretion by different mechanisms. The maximal acid response to histamine was more resistant to inhibition than that to pentagastrin; 0.20 M HCl inhibited secretion by 43%, 1200 mOsm X kg-1 of PEG solution by 42%, and hyperosmolal 0.20 M HCl by 60%. The results suggest that HCl and hyperosmolal solution also inhibit histamine-stimulated secretion by different mechanisms. The anatomical sites of the mechanisms remain to be established.
Explore the source record for details and available documents.
A method of producing chronic gastric fistula and collection of gastric juice in rats. Acta Physiol. Pol., 1978, 29 (1): 79-86. A kind of material suitable for making different parts of the gastric fistula as well as their shape and size have been established. Organic glass (plexiglas) was used for making the cannula. A twisted-on cap of stainless steel protected the mouth of the fistula. This cap secured also the possibility of directly attaching a vessel for collection of gastric juice to the orifice of the cannula. The vessel was made of plexiglas and owing to its shape and dimensions it did not impede the rat's movements during the investigations. A disc of nylon net glued on to the external wall of the cannula prevented leaking of the fistula and its consequences. The fistula produced in this way showed a considerable durability and the vessel made it possible to investigate gastric secretion in a freely moving animal under physiological conditions or under any chosen experimental conditions.
BACKGROUND: Gastro-gastric fistulas and marginal ulcers are frequent and serious complications of gastric compartmentalization procedures for obesity. METHODS: The authors analyzed 810 patients after 911 operations for gastro-gastric fistulas and marginal ulcers over an 8-year period. All patients underwent a form of gastric bypass, in which a pouch is constructed along the lesser curvature of the stomach. The outlet of the pouch was restricted with a prosthetic band. In the first 189 patients (Group I), the pouch and stomach were stapled in continuity or partially divided. In the next 222 patients (Group II), segments were stapled and separated by transection. In the remaining 492 cases (Group III), in addition to transection of the stomach, a limb of jejunum was interposed between the pouch and excluded stomach. Stapled anastomoses were done in Group I and II patients and a portion of Group III patients. The remaining patients underwent hand-sewn anastomosis. RESULTS: Gastro-gastric fistulas occurred in 49% of the patients in Group I, 2.6% of those in Group II, and 0% of those in Group III. In stapled anastomosis, the incidence of marginal ulceration in Groups I, II, and III were 8.5%, 5.4%, and 5.1%, respectively. In a subset of Group III patients, in whom a two-layer, hand-sewn anastomosis was done, the incidence was 1.6% when the outer layer was not absorbable and 0% when both layers were absorbable. CONCLUSIONS: Gastro-gastric fistulas and marginal ulcerations are likely the result of breakdown of the mucosa resulting from migrating staples and other foreign material. Lack of integrity of the gastric lining facilitates the action of the gastric digestive process. Transection of gastric segments with interposition of jejunum prevents gastro-gastric fistula formation. An intact serosa appears to block the digestion of bowel wall by gastric enzymes. Our early data suggest that the use of absorbable sutures at the gastrojejunostomy significantly decreases the incidence of marginal ulceration.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Rats with chronic gastric fistula were used to study gastric and duodenal/pancreatic secretory changes evoked by chemical duodenal ulcerogens. Although the data demonstrate stimulation of gastric output of acid and pepsin by certain doses of cysteamine or propionitrile, cysteamine produced dose-response increases in acid secretion only during the 1st hour following administration. The base output was also elevated at most of the time intervals after cysteamine. Decreased alkaline secretion was only seen following propionitrile injection. Although hyperacidity at the ulcer site may occur during duodenal ulcerogenesis, these results suggest that direct stimulation of acid-pepsin secretion or depression of pancreatic alkaline output are not the primary mechanisms explaining the ulcerogenic action of cysteamine and propionitrile.
In chronic gastric fistula (GF) rats, HCl and a hyperosmolal solution of polyethylene glycol (PEG) in the upper intestine inhibit pentagastrin-stimulated gastric acid secretion by different mechanisms, but their anatomic sites have not yet been established. In the present study GF rats were provided with Thiry-Vella loops of the duodenum and the bile and pancreatic ducts transplanted to the proximal jejunum, or with Thiry-Vella loops of the proximal jejunum. In the latter rats the duodenum was anastomosed as a blind loop to the jejunum to prevent any gastric juice from entering the duodenum. Duodenal loop perfusion with 0.20 M HCl inhibited the acid response to pentagastrin by 62%, but perfusion with 1200 mOsmol x kg-1 of PEG solution did not alter the response. In contrast, acidification of the proximal jejunal loop did not alter but hyperosmolality inhibited the response by 41%. The study shows that the mechanism for inhibition by intestinal acidification is confined to the duodenum and that for inhibition by hyperosmolality is located in the proximal jejunum--but whether only to the proximal part is unknown.
In chronic gastric fistula (GF) rats, hyperosmolal 0.20 M HCl infused into a duodenal loop anastomosed to the jejunum (Roux-en-Y) produced a greater inhibition of the maximal acid response to pentagastrin than HCl or 1200 mosmol kg-1 solution of polyethylene glycol (PEG) alone, suggesting that HCl and hyperosmolal solution inhibit secretion by different mechanisms. In the present study on chronic GF rats with Thirty-Vella loops of the proximal or distal duodenum (bile and pancreatic ducts transplanted to the jejunum), perfusion of the proximal or distal loop with 0.20 M HCl significantly inhibited the maximal acid response to pentagastrin, but perfusion with hyperosmolal PEG solution did not alter the response. The results suggest different anatomical sites for the inhibitory mechanisms, sensitive to acid and hyperosmolal solution.
One to four months after implantation of a gastric fistula, a circadian rhythm in gastric acidity could be demonstrated by use of the intragastric 24-hour pH-metry in dogs with the gastric fistula protruding on the left side of the upper abdomen. This circadian rhythm was found to be fully developed within 3 years, and it remained unchanged up to 5 years after implantation. It is characterized by a daytime intragastric median pH of about 2 and a nocturnal intragastric median pH of about 7. In contrast, a circadian rhythm did not develop within 5 months after instrumentation of the dogs with a gastric fistula protruding on the right side of the upper abdomen. Only 2 years after implantation of the fistula, an intragastric daytime median pH of about 2 and a nocturnal median pH of about 4 appeared. Four years after implantation, the circadian rhythm had evolved. The results show a delayed postoperative restoration of circadian rhythm in canine gastric acidity if a gastropexy occurs at an untolerated position. This may lead to unphysiological distensions in the gastric wall with subsequent continuous stimulation of acid secretion.
Supplementing the food of Heidenhain pouch gastric fistula dogs with a KC1 product greatly extends the survivability of these dogs. Since there is a continuous discharge of gastric juice from the pouch to the exterior each time a meal is consumed, clinical signs such as dehydration, anorexia, rough hair coat and lethargy usually occur within a few months after gastric pouch surgery and, unless extensive supportive measures are taken, most dogs will die shortly thereafter. The five dogs which did not receive KC1 supplementation died within 6 months after surgery with a mean survival time of 2.4 +/- 0.9 months. Seven dogs that received a daily oral supplement of 1.5 g KC1 (20 mEq) in their food have, on average, survived more than ten times longer than dogs which received no KC1 supplementation, with a mean survival time of 25.1 +/- 4.4 months. All KC1 supplemented dogs survived for more than 15 months with three dogs currently surviving for 36-40 months. When two dogs experienced decreased serum potassium, sodium and/or chloride levels and showed clinical signs of electrolyte imbalance despite receiving daily oral KC1 supplementation, intervention with intravenous (i.v.) lactated Ringer's solution and increased amounts of oral KC1 supplement reversed these symptoms within 1-2 weeks. Dogs that received only i.v. Ringer's therapy died with 1 week of the onset of clinical signs. Daily oral KC1 supplementation, careful observation of behavior and eating patterns, and routine physical examinations and serum electrolyte measurements can greatly extend the life expectancy of dogs with Heidenhain pouch gastric fistulas.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.