Paracetamol potentiates stress-induced gastric ulceration in rats

Cho, C H; Ogle, C. W.

doi:10.1111/j.2042-7158.1990.tb06606.x

Cited by 5 publications

(3 citation statements)

References 21 publications

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“…Cold‐restraint administration is a commonly used experimental model to induce acute gastric damage in rats. 1‐6 Although the pathogenesis of gastric lesions in this model is not completely understood, mast cell degranulation, 7‐10 increase in gastric muscular contractility, 1,2,11 diminished mucosal blood flow, release of several biogenic amines, 1‐3,9‐14 activated leukocytes, 2 and lipid peroxidation resulting from free‐radical generation have been suggested to explain the acute gastric damage associated with cold‐restraint stress. Recent studies suggest that oxygen free radicals might be one of the important factors in inducing gastric mucosal injury during stress.…”

mentioning

confidence: 99%

The Protective Effect of Vasoactive Intestinal Peptide (VIP) on Stress‐Induced Gastric Ulceration in Rats

Tunçel

Erkasap

Şahıntürk

et al. 1998

Annals of the New York Academy of Sciences

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The pathogenesis of cold-restraint stress ulcer involves various factors and is not completely understood. Mast cell degranulation, increased gastric muscular contractility, diminished mucosal blood flow, release of several biogenic amines, activated polymorphonuclear leukocytes, and lipid peroxidation which results from toxic oxygen molecules were suggested to be related to the production of gastric damage by cold-restraint stress. Recent evidence strongly indicates that VIP has a modulatory effect on tissue injury. Sprague-Dawley rats were used in two series of experiments. One set of rats was exposed to cold-restraint stress with some of the rats pretreated with VIP. The second set of rats was exposed to cold-restraint stress and then was administered VIP for different durations. Cold-restraint stress induced gastric lesions and mast cell degranulation and also increased lipid peroxidation in gastric tissue. VIP prevented stress-induced ulcers and mast cell degranulation and protected gastric tissue from lipid peroxidation. When VIP was used after induction of stress ulcer it was therapeutically beneficial. Thanks to its antioxidant and anti-inflammatory activity, VIP can be valuable in the prevention of gastric mucosal damage induced by cold-restraint stress.

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mentioning

confidence: 99%

The Protective Effect of Vasoactive Intestinal Peptide (VIP) on Stress‐Induced Gastric Ulceration in Rats

Tunçel

Erkasap

Şahıntürk

et al. 1998

Annals of the New York Academy of Sciences

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“…Using a single-blind method, the area of the total glandular mucosa and the areas of gross haemorrhagic damage were traced on a glass slide and their sizes were estimated by projecting the tracing onto a graph paper [9]. In the indomethacin and stress ulcer models, mucosal damage was directly measured along the ulcer greatest length; in the case of petechiae, five of these were taken as the equivalent of a 1 mm ulcer [15]. The sum of lesion lengths in each group of animals was divided by its number.…”

Section: Measurement Of Lesion Severitymentioning

confidence: 99%

A study of the antiulcer mechanisms of propanolol in rats

Kaan

Cho

1996

Inflamm Res

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Although propranolol has been shown to protect against ethanol and stress ulceration, the antiulcer mechanisms are still unclear. The present study examined the antiulcer mechanisms of propranolol in three different types of ulceration induced respectively by ethanol (60%), indomethacin (30 mg/kg) and stress (cold-restraint). Propranolol pretreatment in the highest dose (10 mg/kg) given either intraperitoneally (i.p.) or orally (p.o.) prevented gastric mucosal damage in these three ulcer models. The three doses of the drug (2.5, 5 or 10 mg/kg) dose-dependently decreased systemic blood pressure which was accompanied by a reduction of gastric mucosal blood flow. These findings suggest that the protection was unrelated to an improvement of local circulation in the stomach. However, propranolol preserved the mucus levels in the three types of ulcer models. The beta-adrenoceptor blocker also increased the basal gastric mucosal potential difference. These findings indicate that propranolol strengthens the mucosal barrier by the preservation of mucosal mucus and enhancement of the mucosal integrity in the stomach.

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“…Using a single-blind method, lesion areas in the ethanol-induced mucosal necrosis were measured as previously described (Woo & Cho 1994). In the indomethacin and stress models, mucosal damage was directly measured along the ulcer length (Cho & Ogle 1990a).…”

Section: Measurements Of Lesion Index and Intramucosal Mucus Levelmentioning

confidence: 99%

Effects of Selective β-Adrenoceptor Antagonists on Gastric Ulceration in the Rat

Kaan

Cho

1997

Journal of Pharmacy and Pharmacology

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Metoprolol and butoxamine, beta-adrenoceptor antagonists which act selectively at the beta 1- and beta 2-adrenoceptors, respectively, have been investigated for their actions on the ethanol, indomethacin and cold-restraint stress ulcer models. Oral administration of butoxamine but not metoprolol significantly attenuated gastric mucosal damage in the three types of ulcer model. Intraperitoneal injection of butoxamine reduced indomethacin ulceration but not that of the other two models. The stimulatory effect of butoxamine on the gastric mucosal potential difference and intramucosal mucus level correlated positively with its anti-ulcer action. Only oral administration of butoxamine significantly increased the mucosal prostaglandin E2 (PGE2) level but not after intraperitoneal injection. Oral administration of butoxamine also significantly increased the mucosal PGE2 level in the three types of ulcer model but this drug was only effective in the indomethacin ulcer model after intraperitoneal injection. Gastric acid and pepsin output were not affected by either drug. Metoprolol significantly reduced systemic blood pressure; this could be attributed to a reduction in gastric mucosal blood flow. These results imply that beta 2-adrenoceptors play a significant role in the pathogenesis of gastric ulceration. We suggest that the anti-ulcer effect of butoxamine was in part a result of strengthening of the mucosal barrier but that this was not effected by modification of acid or pepsin secretions in the stomach. Stimulation of PGE2 in the gastric mucosa could contribute in part to the anti-ulcer action of the drug, especially when given by the oral route.

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Paracetamol potentiates stress-induced gastric ulceration in rats

Cited by 5 publications

References 21 publications

The Protective Effect of Vasoactive Intestinal Peptide (VIP) on Stress‐Induced Gastric Ulceration in Rats

The Protective Effect of Vasoactive Intestinal Peptide (VIP) on Stress‐Induced Gastric Ulceration in Rats

A study of the antiulcer mechanisms of propanolol in rats

Effects of Selective β-Adrenoceptor Antagonists on Gastric Ulceration in the Rat

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