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Biomedical subjects

N S Parmar

Publications and source records attributed to N S Parmar.

50 records · Page 3Linked to original sources

The effect of 3-methoxy-5,7,3',4'-tetrahydroxyflavan on the restraint induced gastric ulceration augmented by aspirin, a gastric mucosal barrier breaker.

The gastric anti-ulcer activity of 3-methoxy-5,7,3',4'-tetrahydroxyflavan (ME), a specific histidine decarboxylase inhibitor, has been studied on a new experimental restraint rat model in which the ulcerogenic effect of 6 h restraint stress was augmented by the prior treatment with 50mg/kg p.o. dose of aspirin. Aspirin is a known gastric mucosal barrier breaker and it produces a significant increase of the ulcer index in the restraint rat model. ME (ED50 22mg/kg) was found to be more potent than cimetidine (ED50 31mg/kg) in this model. The results of this study indicate that ME, which has been shown to possess significant anti-ulcer activity against 24 h restraint, 19 h pylorus ligation and phenylbutazone, aspirin and reserpine induced gastric ulcers, also possesses the potential of protecting the gastric mucosal barrier. The restraint-aspirin model described in this study is simple as compared to other models of stress induced ulceration, moreover, it also implicates the damage of gastric mucosal barrier and thus it can be used for screening the gastric anti-ulcer activity of drugs providing more useful information.

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The gastric anti-ulcer activity of naringenin, a specific histidine decarboxylase inhibitor.

The gastric anti-ulcer activity of a specific histidine decarboxylase inhibitor naringenin, the aglycone of naringin, a naturally occurring flavanone glycoside obtained from kino and grapefruits, has been studied on the various types of ulcers experimentally induced in rats, viz., pylorus-ligated (Shay method) and restraint ulcers, and on the gastric mucosal damage induced by aspirin, phenylbutazone or reserpine. Naringenin possessed significant anti-ulcer activity in all these models, manifesting a dose-dependent anti-ulcer effect on the pylorus-ligated and restraint ulcers. However, the ED50 value against ulcers in the pylorus-ligated rats (132 mg/kg) was significantly greater than that against ulcers in the restraint rats (42 mg/kg). Amongst all the models used, naringenin was found most effective against the restraint rats. It is suggested that a mechanism involving the inhibition of formation and release of endogenous histamine in the gastric mucosa of rats is implicated in the protective effect of naringenin.

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Gastric anti-ulcer activity of (+)-cyanidanol-3, a histidine decarboxylase inhibitor.

The gastric anti-ulcer activity of (+)-cyanidanol-3, a specific histidine decarboxylase inhibitor was studied on various types of experimentally induced ulcers in rats viz., pylorus-ligated and restraint ulcers, gastric mucosal damage induced by non-steroid anti-inflammatory drugs like aspirin, phenylbutazone, indomethacin and ibuprofen and by reserpine. Guinea pigs subjected to histaminee challenge were also used in the study. (+)-Cyanidanol-3 possesses significant gastric anti-ulcer activity in all these models. However, the ED50 values against pylorus-ligated and restraint ulcers and against histamine-induced ulcers in guinea pigs differed significantly from one another. It was most effective against the restraint ulcers in rats. It is suggested that mechanisms involving formation, release or direct antagonism of histamine may be involved in the protective effects of (+)-cyanidanol-3 observed in this study. As its use as an antihepatotoxic drug has already been established, it is worthwhile to consider it for clinical trials in the therapy of human stress ulcers.

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Anticonvulsant action of thiabendazole.

Thiabendazole was found to be specifically effective against maximal electroshock seizures in albino rats. It produced a significant dose-dependent decrease in the duration of the tonic extensor phase of hind legs. The ED50 was similar for oral or s.c. administration. PTZ-induced convulsions were unaffected by lower doses but aggravated by the higher dose studied.

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Effect of nicotine and alcohol pretreatment on the gastric mucosal damage induced by aspirin, phenylbutazone, and reserpine in rats.

The effect of nicotine and alcohol pretreatment by feeding nicotine (2.5 mg/100 ml), alcohol (25%, v/v) and their combination (nicotine 2.5 mg/100 ml + alcohol 25%, v/v) in drinking water ad libitum for 21 days was studied on the gastric mucosal damage induced by aspirin, phenylbutazone, and reserpine in rats. When given alone, neither nicotine nor alcohol produced any visibly discernible gastric lesions. Their concurrent administration, however, produced minor injury to the gastric mucosa appearing as 5-7 circular ulcers of less than 1 mm in diameter. Pretreatment with nicotine, alcohol, and their combination resulted in the significant augmentation of gastric ulcers produced by aspirin, phenylbutazone, and reserpine. The augmentation of gastric lesions in the group pretreated with the combination of nicotine and alcohol was significantly greater than in the groups treated by either of them alone. The effect of nicotine on the mucus neck cell population of the gastric mucosa and pancreatic bicarbonate secretion, and the gastric mucosal damaging effect of chronic alcohol treatment may be responsible for the potentiation of ulcerogenic effects of aspirin, phenylbutazone, and reserpine.

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