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Biomedical subjects

D Aures

Publications and source records attributed to D Aures.

At least 19 recordsLinked to original sources
PubMed1982

Effect of increased gastric mucosal histamine on alcohol-induced gastric damage in rats.

The aim of this study was to determine whether the cytoprotective effect of prostaglandin might be mediated, at least in part, by inhibition of intramucosal histamine release. Intragastric instillation of increasing concentrations of ethanol in 150 mM HCl resulted in increasing lesion scores and increasing histamine release into the gastric content. Pretreatment with 16,16-dimethyl prostaglandin E2 significantly reduced both lesion scores and gastric histamine output. The intragastric instillation of histamine with tracer [14C]histamine either with or after 50% ethanol resulted in significant gastric tissue uptake of histamine and increased acid secretion. However this had no effect on lesion score, protein output or the protective effect of prostaglandin pretreatment. We conclude that the cytoprotective effect of 16,16-dimethyl prostaglandin E2 in the rat is independent of intramucosal histamine release.

Animals↗
PubMed1980

Intravenous indomethacin and aspirin reduce basal gastric mucosal blood flow in dogs.

The effect of two known inhibitors of prostaglandin synthesis, indomethacin and aspirin, on blood flow was studied in six Heidenhain pouch and three antral pouch dogs. The unstimulated gastric mucosa was bathed with 0.15 M HCl and clearance of [14C]-aminopyrine was used as an index of changes in mucosal blood flow. [14C]aminopyrine clearance was measured during three 15-min predrug periods and five 15 min-postdrug periods. Either indomethacin (10 mg . kg-1), aspirin (100 mg . kg-1), or 0.15 M NaCl were given intravenously as a bolus. Indomethacin reduced mucosal blood flow in the Heidenhain pouch 52% (P less than 0.05) and in the antral pouch 52% (P less than 0.05). Aspirin reduced Heidenhain pouch mucosal blood flow 31% (P less than 0.05). Indomethacin caused no significant change in electrical potential difference or in net flux of H+ or Na+ in Heidenhain pouches. Indomethacin (10 mg . kg-1 iv) produced no change in mean arterial pressure. We conclude that indomethacin and aspirin reduce unstimulated gastric mucosal blood flow, suggesting that endogenous prostaglandin may contribute to its maintenance.

Animals↗
PubMed1979

Topical aspirin plus HCl gastric lesions in the rat. Cytoprotective effect of prostaglandin, cimetidine, and probanthine.

The effect of representative agents of three classes of antisecretory compounds; prostaglandins, histamine H2-receptor antagonist, and anticholinergic agents, on acute gastric mucosal lesions produced by topical aspirin (200 mg/kg) plus HCl (150 mM) in the pylorus-ligated rat was studied. Acid was given exogenously so as to negate any antisecretory effect of the drugs studied. Both nonantisecretory and antisecretory doses of each agent as determined by preliminary secretory studies were employed. The postaglandin analogue 16,16-dimethyl prostaglandin E2, the H2-receptor antagonist cimetidine, and the anticholinergic agent probanthine, in both doses studied, all significantly reduced lesion formation. The H1-receptor antagonist mepyramine neither protected by itself nor enhanced the protective effect of cimetidine. Pepsin release into the gastric content increased with increasing mucosal damage. However, addition of pepsin to the gastric instillate had no effect on severity lesions in any group, which indicates that the increased pepsin was the result of, and not the cause of, the mucosal damage. The findings indicate that all three classes of antisecretory agents studied are also cytoprotective, i.e., they can protect against gastric mucosal injury by topical aspirin plus HCl by some mechanism other than inhibition of acid and pepsin secretion.

Animals↗
PubMed1979

Effects of prostacyclin and a stable analogue, 6-beta-PGI1, on gastric acid secretion, mucosal blood flow, and blood pressure in conscious dogs.

We studied the effect of prostacyclin, PGI2, its chemical decomposition product, 6-oxo-PGF1 alpha, and a stable 5-6-dihydro analogue, 6-beta-PGI1, on gastric acid secretion, mucosal blood flow (14C-aminopyrine clearance), and mean arterial pressure in unanesthetized dogs. During submaximal acid secretion from a gastric fistula induced by intravenous histamine dihydrochloride (20 microgram kg-1 h-1), prostacyclin and its stable analogue, 6-beta-PGI1, reduced acid output with ID50s (dose causing 50% inhibition) of about 0.2 and 3.0 microgram kg-1 min-1 i.v., respectively, whereas 6-oxo-PGF1 alpha was inactive at 100 times the effective dose of prostacyclin. The ratio of mucosal blood flow to acid output remained unchanged during prostacyclin administration and was significantly elevated during 6-beta-PGI1 infusion, suggesting that with both compounds the changes in mucosal blood flow were not the cause of the antisecretory action. For doses causing equivalent antisecretory action, 6-beta-PGI1 lowered systemic arterial blood pressure much less than prostacyclin, indicating selectivity of action. Prostacyclin is unlikely to be a circulating antisecretory agent, but may play a role as a local humoral modulator of secretion and blood flow in the gastric mucosa.

Aminopyrine↗
PubMed1978

Histamine augments gastric ulceration produced by intravenous aspirin in cats.

In unanesthetized cats, continuous intravenous infusion of aspirin for 36 hr did not produce gastric ulcers when given alone but did when combined with 160 microgram kg-1 hr-1 of histamine-2HCl intravenously. The ulcers were mainly antral in location. The incidence and severity of ulcers increased with duration of the infusion up to 36 hr and with dose of aspirin up to 4 mg kg-1 hr-1. With the highest doses and longest durations some of the antral ulcers perforated. Antral ulcers occurred in more than half of the cats getting 0.25 mg kg-1 hr-1 or more of aspirin for 36 hr or getting 4 mg kg-1 hr-1 of aspirin for 6 or more hr. Intravenous aspirin plus intragastric infusion of 40 ml hr-1 of 150 mM HCl for 16 hr also produced gastric ulcers. Plasma salicylate concentrations were less than 350 microgram ml-1 with all doses and durations of aspirin used (400 microgram ml-1 is regarded as the upper limit of the therapeutic range in man). These studies show that when the stomach is acidified by giving histamine intravenously or HCl intragastrically, intravenous aspirin produces large deep gastric ulcers. The mechanism of the ulcerogenic action of intravenous aspirin is not known.

Animals↗
PubMed1976

Mechanism of prevention of aspirin-induced gastric lesions by bile duct legation in the rat.

UNLABELLED: Gastric reflux of bile has been reported to be essential for the production of acute gastric mucosal lesions by intragastric aspirin in the rat. The purpose of the present study was to determine whether bile duct legation of pylorus ligation in the rat inhibits asprin-induced gastric lesions, and, if so, what the protective mechanisms are. Operations were performed under ether anesthesia. Asprin, 200 mg per kg, was instilled into the stomach 1/2 hr postsurgery (bile duct ligation or pylorus ligation). Four hours later the rats were killed, the stomachs were examined, and mucosal lesions were scored. Bile duct ligation, but not pylorus ligation, significantly protected against aspirin-induced gastric-lesions. Bile duct ligation, in pylorus-ligated rats, inhibited gastric acid output by 78%. Instilling HCl + aspirin in bile duct-ligated rats restored lesion formation. Shunting bile to the colon (to prevent bile reflux) did not prevent aspirin lesions. Salicylate determination, to ascertain whether bile duct ligation altered asprin absorption, revealed no significant differences between bile duct ligation and aspirin, shunt + aspirin, and sham shunt + aspirin in plasma and gastric tissue salicylate concentrations. CONCLUSIONS: (1) Bile duct legation protects against aspirin-induced gastric mucosal lesions by inhibiting gastric HCl secretion. As a corollary, a certain amount of acid in the stomach is necessary for aspirin-induced gastric lesions to form. (2) Bile reflux is not necessary for aspirn-induced gastric lesions in the rat.

Animals↗
PubMed1976

Gastric mucosal lesions produced by intravenous infusion of aspirin in cats.

Aspirin was given by continuous intravenous infusion to 35 intact cats for 7 days in doses ranging from 25 to 200 mg kg-1 day-1. Gastric mucosal lesions occurred in 50 to 70% of the animals in the various dosage groups, including deep ulcers in 20%. All of the ulcers were in antral mucosa near its border with oxyntic mucosa. The incidence of lesions, including ulcers, showed no apparent relation to the dose of aspirin. With all but the highest dose, plasma salicylate levels were within or below what is regarded as the therapeutic range for man. Asprin, 100 mg kg-1 day-1, was given for 7 days to 4 cats with pouches containing all of the antral mucosa plus some oxyntic mucosa. One or more deep ulcers occurred in the antral mucosa of the pouches in each of these 4 cats. The electrical potential difference across the mucosa did not decrease, and net fluxes of hydrogen ions out of the pouch and of sodium ions into the pouch did not increase during the 7 days of aspirin administration despite the occurrence of ulcers in the pouches. It is concluded that intravenous aspirin, in doses giving plasma levels within or below the therapeutic range for man, causes gastric mucosal lesions including deep ulcers within 7 days in cats. These lesions occur without the changes in electrical potential difference and hydrogen and sodium fluxes that are regarded as characteristic of the "broken barrier."

Animals↗