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H S Himal

Publications and source records attributed to H S Himal.

At least 55 records · Page 3Linked to original sources
PubMed1981

Prevention of sepsis-induced gastric lesions in dogs by cimetidine via inhibition of gastric secretion and by prostaglandin via cytoprotection.

The cytoprotective and acid-inhibitory effects of cimetidine and 16,16-dimethyl PGE2 were evaluated in a septic canine erosive gastritis model. In 21 dogs, total gastric fistulas were created, and after a 3-wk recovery period, basal, food-, and pentagastrin-stimulated acid output were measured. Then bacterial peritonitis was created by the intraperitoneal instillation of Pseudomonas, Bacteroides, Streptococcus Fecalis, Klebsiella and canine gallbladder bile. In 5 dogs no drug were given throughout the septic period while in 16 dogs either cimetidine, 6 or 12 mg/kg i.m. every 6 h, or 16,16-dimethyl PGE2, 0.2 or 0.4 microgram/kg i.m. every 6 h, was given 24 h before the induction of peritonitis and continued for 3 days. All 21 dogs had positive blood cultures on the 1st septic day. In the control animals, basal, food-, and pentagastrin-stimulated acid output significantly increased during the first 2 septic days, and gastroscopy demonstrated bleeding acute fundic erosions. Cimetidine decreased basal, food-, and pentagastrin-stimulated acid output in a dose-related manner, and only with the higher dose did it prevent gastric mucosal damage. 16,16-Dimethyl PGE2, 0.4 microgram/kg, significantly decreased acid output and prevented gastric mucosal damage. 16,16-Dimethyl PGE2 0.2 microgram/kg, although having no apparent effect on basal, food-, and pentagastrin-stimulated acid output, prevented the development of acute gastric erosions. Thus, in the canine septic model, acid output significantly increases during sepsis. Cimetidine prevents the development of sepsis-induced gastric erosions by inhibition of acid secretion and 16,16-dimethyl PGE2 by cytoprotection.

Animals↗
PubMed1980

The role of mucus glycoproteins in prostaglandin cytoprotection.

The role of gastric mucus in the pathogenesis of septic erosions and as an explanation for prostaglandin cytoprotection is unclear. In a reproducible canine septic model bacterial peritonitis was induced in three groups of dogs. One group served as a control and each of the remaining groups received 16,16 dimethyl PGE2 either 0.2 microgram/kg. or 0.4 microgram/kg. I.M. q6h beginning 24 hours prior to peritonitis and continued during the septic period. Gastroscopy was performed and basal gastric juice collected prior to peritonitis and during the septic period. All animals in the control group developed acute gastric erosions and gastric juice protein significantly decreased while sialic acid and fucose significantly increased during the septic period. In the animals receiving 16,16 dimethyl PGE2 acute gastric erosions did not develop; sialic acid and fucose were significantly elevated compared to control dogs during sepsis. We conclude that prostaglandin cytoprotection may be related to increases in gastric glycoprotein secretion.

Animals↗
PubMed1978

Upper gastrointestinal hemorrhage: aggressive management decreases mortality.

In a retrospective study of 630 patients with upper gastrointestinal hemorrhage admitted to the Royal Victoria Hospital between 1963 and 1971, the overall mortality was 12.54%. Mortality increased in patients receiving more than 10 units of blood and in patients over 60 years of age. Mortality decreased in patients in whom the site of hemorrhage was known prior to operation. Early surgery for gastric ulcers and conservative therapy for acute gastric erosions reduced mortality. Therefore in 334 patients admitted to the Royal Victoria Hospital between 1973 and 1976 with upper gastrointestinal hemorrhage, an aggressive approach to diagnosis and management was emphasized. There was a significant decrease in patients with duodenal ulcers, acute gastric erosions, and gastric ulcers who received more than 10 units of blood. There was a significant increase in the use of endoscopy to establish the source of hemorrhage and a significant increase in the use of endoscopy to establish the source of hemorrhage and a significant decrease in the number of patients who did not have a diagnosis prior to operation. There was also a significant increase in early surgery for gastric ulcers. This regimen led to a significant decrease in mortality (6.69% vs. 12.54%). This report demonstrates that early diagnosis and management based on the lesion found reduces mortality from upper gastrointestinal hemorrhage.

Blood Transfusion↗
PubMed1977

Antral gastrin and acid secretion in duodenal ulcer patients.

By means of intragastric instillation of meat extract, two groups of duodenal ulcer patients were identified--antral responders and antral nonresponders. Antral response was abolished ater vagotomy and drainage or vagotomy-antrectomy. The differentiation would allow for selective surgery for duodenal ulcer patients.

Drainage↗
PubMed1977

Acid absorption in the canine duodenum.

Alterations in composition of isosmotic acid solutions were studied in exteriorized segments of the proximal (Brunner's gland area) and distal canine duodenum, mounted in lucite chambers. Varying concentrations of HCl (40, 80, 120, 160 mEq/l) made isotonic by the addition of NaCl were instilled into the chamber, removed in 15 minutes and analyzed for volume, electrolytes, protein content and osmolality. Both proximal and distal duodenal mucosa modified the instilled solution with a loss of H+ and a gain in Na+ and K+, which occurred at similar rates independent of the acid concentration of the instilled solution. The rate of ionic movement was twice that for the antrum, and 30-100 times that of the fundus. Calculated H+ loss across the entire duodenal mucosa at these rates could account for 17.5% of the peak acid output from the canine stomach. The loss of H+ could not be accounted for on the basis of neutralization and probably represented transmucosal insorption. In addition to the neutralization of gastric acid by pancreatic juice and bile, duodenal mucosa thus plays an important role in the maintenance of intraluminal pH. Duodenal mucosal permeability to H+ may be related to the vulnerability of the duodenal mucosa to acid-peptic ulceration.

Animals↗
PubMed1977

Ionic flux across canine duodenum. Movement of bicarbonate.

Effect of isosmotic biocarbonate-rich solutions on the Brunner's gland area were studied by means of proximal duodenal explants in eight anesthetized dogs. Volume gain occurred with all instillates and varied indirectly with the concentration of the bicarbonate in the instilled solutions. Net bicarbonate gain occurred with instillate of 40 mEq./1.; net insorption occurred with instillates of higher bicarbonate concentration, the rate of which was dependent on the instillate concentration. Insorption of chloride occurred with the lower bicarbonate solutions and enterosorption occurred at higher concentrations. The modification of intraluminal bicarbonate by the proximal duodenal mucosa is important in the regulation of intraduodenal pH and abnormal function of this mechanism may play a role in the pathogenesis of duodenal ulceration because of incomplete hydrochloric acid neutralization.

Animals↗
PubMed1977

The effect of ethanol and bile on electrolyte movement across canine proximal duodenal mucosa.

The existence of a gastric mucosal barrier, controlling H+ N+ flux has been well established. The disruption of this barrier by ethanol and bile has also been confirmed. This study was designed to investigate the effect of ethanol and bile on the duodenal mucosa, which, as we have shown, is similar to gastric mucosa in that there is H+, Na+ flux. In 10 dogs, duodenal explants with an intact blood supply were placed within lucite chambers. Under basal conditions there was H+ insorption and Na+ exsorption. Neither bile nor ethanol caused increased H+ Na+ flux. Acute erosions did not develop in the proximal duodenum, as has been shown to occur when bile or ethanol is instilled into the stomach. These studies, therefore, demonstrate that although H+ Na+ occurs across the duodenal mucosa, bile or ethanol do not cause changes in ionic flux and acute erosions do not develop.

Animals↗
PubMed1977

Alkaline gastritis and alkaline esophagitis: a review.

Alkaline gastritis and alkaline esophagitis are now precisely defined syndromes. They occur most often after gastric surgery in which function of the pyloric and lower esophageal sphincter is compromised. Reflux of bile in these patients can then lead to severe inflammation of the gastric and lower esophageal mucosa. Epigastric pain, nausea and bilious vomiting are characteristic symptoms. Gastroscopy with biopsy is, therefore, the definitive diagnostic test; during endoscopy bile is seen in the lower esophagus or stomach, and the mucosa is red, friable and contains acute erosions. Conservative therapy including the administration of cholestyramine has not been helpful. Surgery consisting of diversion of the duodenal contents away from the stomach and lower esophagus is the treatment of choice. The Roux-en-Y procedure has been used most often and has resulted in the amelioration of the symptoms and signs in most patients.

Animals↗
PubMed1977

Effect of antrectomy and vagisecretion on gastric acid output and gastrin secretion.

In three dogs with denervated Heidenhain pouches, ingestion of cooked beef liver caused increased acid output and gastrin secretion. After antrectomy and gastrojejunal anastomosis, ingestion of the liver did not increase serum gastrin levels throughout the experiment. Acid output, however, although markedly reduced, was elevated over basal levels during the last three hours of the four-hour experiment. Total abdominal vagotomy did not alter gastrin secretion but further inhibited acid output in response to the test meal. These results indicate that in the dog intestinal gastrin is not released in response to a beef liver meal. Acid output postantrectomy, although reduced, does respond to the meal and is further decreased after vagotomy. A hormonal mechanism other than the release of intestinal gastrin is responsible for the intestinal phase of gastric acid secretion.

Abdomen↗
PubMed1977

Management of perforating diverticulitis of the colon.

A retrospective study was carried out of all patients admitted to the hospital with either local or free perforating diverticulitis. Fifty-one patients had perforating diverticulitis of the sigmoid colon with local abscess formation, while 26 patients had free perforation with generalized peritonitis. Of the 67 patients who had a defunctioning colostomy, 18 died, while of ten patients who had either resection or exteriorization of the perforated segment, one died. Thus, exteriorization or resection as the primary surgical procedure for perforating diverticulitis is the procedure of choice, since it leads to a low operative mortality because of removal of the septic focus, preventing continuing intraperitoneal soilage.

Colostomy↗
PubMed1977

The relationship between antral function and completeness of vagotomy.

To assess whether or not a persistent antral response to meat extract stimulation is an indication of incomplete vagotomy, 29 patients with a duodenal ulcer who underwent operation had preoperative and postoperative acid studies as well as postoperative Hollander tests. In the preoperative tests, two groups of patients were delineated--antral and nonantral responders. Postoperative Hollander tests revealed three positive responses; in two patients with an early positive response, meat extract led to a significant increase in acid and gastrin response. In the patient with a late positive Hollander test, there was no response to meat extract. In two patients with proved stomal ulcers and negative Hollander tests, meat extract led to a significant increase in acid and gastrin output. These results suggest that an antral acid and gastrin response to meat extract indicate an incomplete vagotomy.

Drainage↗
PubMed1977

Effect of bile on lysosomal stability in the mucosa of the canine gastric antrum.

The bound and free acid hydrolases from bile and bile- then acid-treated canine antral mucosa were compared with control tissue, using explants held in a series of Lucite chambers. Normal levels of activity of bound mucosal enzymes decreased as a result of bile acid insult, but "free" activity in the cytosol increased markedly. Organelle membrane stability was "tested" by submitting isolated particulate matter containing lysosomes, to hypoosmotic shock and to mechanical stress. Release of cathepsin D, only, was observed after bile treatment in vivo. Bile, followed by acid, however, damaged organelle integrity causing release or "leakage" of seven acid hydrolases.

Animals↗
PubMed1976

Establishment of the integrity of lysosomes in a glycoprotein-rich matrix. Distribution pattern of seven lysosomal enzymes in gastric mucosa.

Gel-forming mucosal glycoproteins strongly interfere with standard methods of cell fractionation. Thus, acid hydrolase-bound particles imbedded in the gel, sediment on centrifugation, in the nuclear fraction of homogenates of canine antral mucosa. These particles can be cleared by direct solubilization of the gel; however, the viscosity of the solution obtained prevents sedimentation of some of the latent hydrolases, even at very high speeds. The use of a new step-wise scheme of centrifugation and dilution successfully isolates lysosomal particles containing acid hydrolases from mucin-rich mucosa. All of the enzymes investigated, including acid phosphatase, cathepsin D, alpha- and beta-galactosidase, beta-B-acetylhexosaminidases, but with the exception of alpha-fucosidase, were found to be particle bound, exhibiting high degrees of latency. However, active mucosal particles are polydisperase in size and density, sedimenting under different centrifugal forces.

Acetylglucosaminidase↗
PubMed1976

The effect of vagotomy antrectomy or vagotomy pyloroplasty on the response of the antrum to meat extract in duodenal ulcer patients.

In 9 normal and 42 duodenal ulcer patients, acid and gastrin studies were performed. Basal, Oxo and Histalog stimulated acid secretion was conducted on each patient. In 24 patients post vagotomy pyloroplasty or vagotomy antrectomy, these studies were repeated within three months after surgery. Two groups of duodenal ulcer patients were identified; those who did respond and those who did not respond to Oxo stimulation. In the "responders," Oxo stimulated acid output and gastrin secretion increased significantly over basal values. Both vagotomy pyloroplasty and vagotomy antrectomy caused a similar significant decrease in Oxo and Histalog stimulated acid output. In two patients with incomplete vagotomy, antrectomy, but not pyloroplasty abolished the Oxo stimulated acid response. These data suggest that OXO stimulation test can select patients with a significant antral component in whom vagotomy and antrectomy would be the appropriate procedure. Our results also indicate that antrectomy will protect against recurrent ulceration in patients with incomplete vagotomy and may explain the lower incidence of stomal ulceration in patients with vagotomy antrectomy, compared to vagotomy pyloroplasty.

Drainage↗