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.

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.

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.

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.

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.

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.

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.