Healing Of Chronic Gastric Ulcers Research Articles

Irritative activity of antiinflammatory agents, betamethasone 17-valerate, beclomethasone 17, 21-dipropionate, betamethasone 17, 21-dipropionate, or indomethacin on the gastrointestinal tract in rats and dogs (author's transl)

Irritative effects of three steroidal anti-inflammatory drugs on the gastrointestinal tract of rats and dogs were determined. With either single or repeated subcutaneous administration these drugs dose dependently irritated the gastric mucosa of both species. The intestinal mucosa was less affected. Concomitant oral administration of aspirin or subcutaneous administration of indomethacin revealed an aggravation of aspirin-induced gastric ulcers by betamethasone valerate and inhibition of indomethacin-induced intestinal ulcers by beta-methasone dipropionate. These two steroidal drugs had no noxious effect on healing of chronic gastric ulcers induced in rats and dogs. Betamethasone valerate, however, delayed the healing of gastric ulcer in rats. Indomethacin, a non-steroidal anti-inflammatory drug, also induced serious damage to the gastric and intestinal mucosa both of rats and dogs. Indomethacin ingestion delayed the healing of chronic gastric ulcer in rats but not in dogs. Since both steroidal and non-steroidal drugs induce damage to the gastrointestinal tract, a careful monitoring of the patients' complaints should be carried out when these compounds are used as a systemic treatment. Steroidal drugs used in this study, however, appear to be highly safe from the point of dose inasmuch as they are used as a topical treatment.

INFLUENCE OF SURGICAL SYMPATHECTOMY ON GASTRIC SECRETION AND ULCERATION IN RATS

The influences of sympathectomy on gastrointestinal mucosa, gastric secretion, acute or chronic gastric ulcers were studied in rats. Uncer ether anesthesia, sympathectomy was performed by surgical removal of the celiac ganglion. Surgical sympathectomy per se produced no pathological changes in the gastrointestinal tract as determined by macroscopical observation 3, 10 or 20 days after operation. The volume of gastric juice and pepsin output were not influenced by the sympathectomy but gastric acid output was significantly increased in pylorus-ligated rats. The sympathectomy worsened the stress- and the indomethacin-induced ulcer and delayed the healing of chronic gastric ulcers a little but not significantly, and had no deteriorative influence on the reserpine-induced ulcers. In contrast, Shay ulcers, aspirin- or secrotonin-induced ulcers were significantly aggravated by sympathectomy. The loss of H+ ions and gain of Na+ ions in the gastric juice of pylorus-ligated and aspirin-treated rats were not affected by sympathectomy.

Influence of aspirin on healing of chronic gastric ulcers in dogs.

Gastric ulcers induced in dogs by transserosal injection of 1 ml of 40% acetic acid healed completely by the 7th week after ulceration and never reulcerated during the observation period up to 12 weeks. Acetic acid ulcers in the active (at 1 week), quiescent (3 weeks) or healed (at 7 weeks) stages were not influenced by the daily administration of aspirin 2 g/dog/day for for 5 consecutive weeks. All examinations were done by gastroscopy in addition to macroscopical and histological observations at autopsy.

Effects of carbenoxolone Na on acute and chronic gastric ulcer models in experimental animals.

Effects of carbenoxolone Na on acute or chronic types of gastric lesions or ulcer models produced in rats, guinea pigs, or dogs were studied. Carbenoxolone Na, given either orally or intraperitoneally, produced a significant inhibition of stress-induced gastric lesions in intact or in pylorus-ligated rats. Acetylsalicylic acid (ASA)-induced or serotonin-induced gastric lesions in rats were also inhibited significantly by pretreatment with the drug. However, carbenoxolone Na did not affect the development of Shay ulceration in rats even though the peptic activity in gastric juices was markedly reduced by the drug. Histamine-induced gastric lesions in guinea pigs were not prevented by pretreatment with carbenoxolone Na. Although carbenoxolone Na, given for 10-20 days, did not promote the healing of stress-induced gastric lesions and acetic acid gastric jlcers in rats, it significantly accelerated the healing of chronic gastric ulcer produced in dogs by 3 weeks' treatment. Carbenoxolone Na prevented the acid back-diffusion caused by ASA without any influence on Na+ efflux in pylorus-ligated rats.

Effects of propantheline bromide and milk plus cheese on healing of chronic gastric ulcers in rats.

Chronic gastric ulcers were produced by intramural injection of 20% acetic acid (0.14 ml) in rat stomachs in order to determine the effects of an antisecretory agent and a bland diet on ulcer healing processes. The effective dosage of propantheline bromide as a gastric secretory inhibitor was determined with chronic fistula rats and found to be 3 mg/kg IP, administered 3 times/day. Propantheline bromide, when given for 32 days beginning from the eighth day after operation, significantly delayed the healing and did not prevent the reexacerbation commonly observed with this type of lesion. Milk and cheese were given as substitutes for conventional rat chow and water for the same test periods as propantheline bromide, and they were found to be associated with a delay in healing during the early phase of ulceration but to prevent to some extent its recurrence.

Glycopyrronium Bromide In The Treatment Of Chronic Gastric Ulcer

The initial healing of chronic gastric ulcer in the hospital was studied in two groups of 20 patients, one treated with bed rest and antacids as required, and one given the same therapy with the addition of glycopyrronium bromide. The anticholinergic drug, Robinul (glycopyrronium bromide), was shown to accelerate the initial healing of chronic gastric ulceration in this group of hospital inpatients. It is suggested that glycopyrronium bromide given in maximum tolerated doses might be an effective addition to present inpatient therapy of chronic gastric ulceration. It was shown in a controlled long term study of outpatients that glycopyrronium bromide protected against gastric ulcer recurrence in those patients who were not salicylate users. People who regularly took salicylates gained no protection from the anticholinergic drug as regards gastric ulcer recurrence. The protective effect of the anticholinergic agent appeared within 6 months and was sustained for 1 and probably for at least 2 years.