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PubMed1988

Effect of calcium channel blocker diltiazem on cytoprotection and prostaglandin and sulfhydryl production by rat gastric epithelial cells.

The calcium channel blockers verapamil and diltiazem protect gastric mucosa against exogenous injury in vivo. Whether this protection is mediated by systemic factors, such as blood flow, is due to inhibition of gastric acid secretion, or is associated with stimulation of endogenous protective agents such as prostaglandins or sulfhydryls, is unknown. We have evaluated whether diltiazem protects rat gastric epithelial cells in tissue culture (a model which excludes the influence of systemic factors) against damage induced by sodium taurocholate, indomethacin, or ethanol. Further we have assessed the effect of diltiazem on prostaglandin and sulfhydryl production. 51Chromium release assay and phase contrast microscopy have been used to assess cell damage. Sodium taurocholate, indomethacin, and ethanol-damaged cultured cells in a dose-dependent manner. Pretreatment with diltiazem did not prevent the drug-induced damage. Diltiazem did not increase PGE2 and 6-keto PGF1a production by cultured cells nor did it affect the cellular level of endogenous sulfhydryls. In conclusion, the calcium channel blocker diltiazem is not directly protective to rat gastric mucosal cells in vitro. Diltiazem does not stimulate prostaglandin production by gastric cells nor does it increase the cellular level of protective sulfhydryls.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Treatment of peptic ulcers--acid reduction or cytoprotection?

In a Swedish multicenter double blind trial cimetidine was compared to sucralfate in the treatment of peptic ulcer. Patients with endoscopically verified gastric, prepyloric and duodenal ulcers were treated with cimetidine 400 mg x 2 or sucralfate 1 g x 4 for four to eight weeks. Gastric ulcers were treated up to 12 weeks. Patients with healed ulcers were followed for up to 12 months. During follow-up without any anti ulcer treatment control endoscopy was performed 2-4 and 9-11 months after endoscopic healing and at symptomatic recurrence. 647 patients were studied (334 cimetidine and 313 sucralfate). 258 patients were included in the 12 months' follow up: of these 143 were previously treated with cimetidine and 115 with sucralfate. Healing rates were 92% in patients treated with cimetidine and 87% in those given sucralfate (ns). Symptomatic relief and ulcer recurrence did not differ between the treatments. Smoking significantly increased recurrence rate and shortened the time to recurrence in the cimetidine treated patients, but not in the sucralfate group. Cimetidine and sucralfate compared well in all aspects of acute peptic ulcer treatment and recurrence during one year of follow up.

Adult↗
PubMed1988

Gastric anti-ulcer and cytoprotective effect of vitamin E in rats.

Effect of vitamin E on the gastric mucosal damage induced by hypothermic restraint stress, indomethacin, reserpine, hydrochloric acid, sodium chloride and ethanol has been studied in rats. The results demonstrate that pretreatment of animals with vitamin E produces a significant inhibition of gastric lesions induced by above mentioned agents. An increase in the synthesis of prostaglandins, and high level of glutathione in tissues of vitamin E treated animals have been suggested as a possible mechanism of anti-ulcer activity of -tocopherol. However, further studies are required to confirm these effects and to determine the role of vitamin E in the prophylaxis and treatment of peptic ulcer disease.

Animals↗
PubMed1988

Prostaglandin cytoprotection in man: effectiveness of rosaprostol.

We studied the effect of a new prostaglandin analogue, 9-hydroxy-19,20-bis-norprostanoic acid (rosaprostol), on the duodenal mucosa of humans after administration of 40% ethanol. Eighteen healthy volunteers entered the study, which followed a blind cross-over design. At time 0 all the volunteers received rosaprostol or placebo; 5 minutes later, 40% ethanol (50 ml dose) was given. The mucosa was examined for lesions 3, 60 and 180 min later under endoscopy, light and scanning microscopy. It was found that: (i) 40% ethanol damaged the duodenum, with blood extravasation, inflammation and necrosis of the mucosa, (ii) rosaprostol significantly protected the mucosa 3 min after 40% ethanol, and (iii) the damage became worse after 3 h when placebo was given, whereas it was reduced after 1 h when PG was administered. The results suggest that PGs not only protect the mucosa against ethanol damage, but also stimulate its recovery.

Adolescent↗