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Biomedical subjects

R S D'Souza

Publications and source records attributed to R S D'Souza.

10 recordsLinked to original sources
PubMed1992

Protective effect of propranolol on ethanol-induced gastric lesions in rats: probable mechanism of action.

The non-selective beta-adrenoceptor antagonist, propranolol, has been reported to protect against gastric injury in mice, an effect only partly due to prostaglandin release. This study was designed to confirm the gastric cytoprotective effect of propranolol in another species of animal, the rat, and investigate further its mechanism of action. Our results show that propranolol prevents both ethanol-induced gastric lesions as well as ethanol-induced contraction of the circular muscle of rat fundic strip. The local anaesthetic, lignocaine also inhibited the effect of ethanol on circular muscle. However, timolol, another non-selective beta-adrenoceptor antagonist, failed to produce such an action. The effect of propranolol was abolished by the cyclooxygenase inhibitor, indomethacin and a high dose of the guanylate cyclase inhibitor, methylene blue. The results suggest that in addition to prostaglandins, endogenous nitric oxide and the membrane stabilising action of propranolol may also be involved in its gastroprotective action.

Animals↗
PubMed1991

Dual action of clonidine on ethanol-induced gastric lesions: is the imidazoline-preferring receptor involved?

The imidazole alpha 2-adrenoceptor agonist, clonidine, exerts a dual action on ethanol-induced gastric lesions. At lower doses, it has a gastroprotective effect which is also seen with two other alpha 2-adrenoceptor agonists - the catecholamine, alpha-methyldopa and the guanidine, guanabenz. The gastroprotective action of the three drugs is prevented by the selective alpha 2-adrenoceptor antagonist, yohimbine, suggesting that the action is mediated by alpha 2-adrenoceptors. However, at higher doses clonidine aggravates ethanol-induced gastric lesions, an effect also seen with another imidazole, oxymetazoline. The aggravating action is not prevented by yohimbine and is not seen with alpha-methyldopa and guanabenz. This suggests that it involves a receptor/mechanism other than alpha 2- possibly an imidazoline-preferring receptor but further work, including radioligand binding studies, is needed to confirm this.

Adrenergic alpha-Agonists↗
PubMed1991

Gastric cytoprotection.

The term 'cytoprotection' means protection against gastric mucosal injury by a mechanism other than inhibition or neutralisation of gastric acid. Several mechanisms of gastric cytoprotection have been proposed like increased mucus and bicarbonate secretion, strengthening of gastric mucosal barrier, increased gastric mucosal blood flow, decreased gastric motility, increased formation of prostaglandins and sulfhydryls, scavenging of free radicals, stimulation of cellular growth and repair, decreased release of leukotrienes etc. Some of the drugs widely used in therapy of peptic ulcer are cytoprotective e.g. sucralfate, colloidal bismuth and aluminium containing antacids. As the concept of gastric cytoprotection is becoming widely accepted, the list of drugs which have shown a cytoprotective action in animal experiments is growing rapidly. This list includes zinc sulphate, meciadanol, propranolol, dipyridamole etc.

Gastric Mucosa↗
PubMed1990

Aggravating action of clonidine on ethanol-induced gastric lesions: probable mechanism of action.

Large doses of the imidazoline alpha 2 adrenoreceptor agonist clonidine aggravate ethanol-induced gastric lesions. The alpha 2 adrenoceptor antagonist phentolamine, the opioid antagonist naloxone and the H2 antagonist cimetidine do not prevent this action of clonidine suggesting that it is not mediated by alpha 2, opioid or H2 receptors. Further, like clonidine, high doses of phentolamine and cimetidine aggravate gastric lesions per se, suggesting that all three may be acting at a common 'receptor' site, possibly the imidazoline-preferring receptor (IPR).

Animals↗
PubMed1990

Comparison of the effects of captopril and enalapril on oxyphenbutazone and ethanol-induced gastric lesions in rats.

We have compared the effect of the converting enzyme inhibitors, captopril and enalapril, on two models of gastric ulcers, viz; ethanol and oxyphenbutazone-induced lesions in rats. Both captopril and enalapril did not affect ethanol-induced lesions. While captopril significantly protected against oxyphenbutazone-induced lesions, enalapril aggravated the lesions. This difference is probably due to the lack of the protective sulfhydryl group in the chemical structure of enalapril.

Animals↗
PubMedDate not supplied

Vascular desensitisation--possible role of prostaglandins.

Prolonged exposure to noradrenaline (NA) brings about an increase in the release of prostaglandin (PG)-like material from rat aortic strip. The release is greater with oxymetazoline while methoxamine decreases it. These effects are blocked by yohimbine and prazosin respectively. Pretreatment with 6-OHDA or reserpine diminishes the release of PG-like material. Barium chloride, a non-specific spasmogen, does not affect the release significantly. It appears therefore that the source of PG-like material is presynaptic and that its release mechanism is linked to an alpha 2 (alpha 2) adrenoceptor. It is proposed that this release of PG-like material contributes to the development of desensitisation in vascular tissue.

Animals↗
PubMedDate not supplied

Gastric cytoprotective effect of morphine is probably not mediated by mu-receptors.

Morphine has a significant protective effect on ethanol-induced gastric lesions. This effect is antagonized by naloxone, suggesting that it is mediated by opioid receptors. In the rat, mu-receptors have been shown to be involved in other gastrointestinal actions of opioids. However, the potent partial agonist at mu-receptors, buprenorphine, not only failed to protect but actually aggravated ethanol-induced lesions at higher doses. The gut-selective mu-agonist, loperamide, also did not have a protective effect, while the mixed opioid, pentazocine, which has an antagonistic action at mu-receptors, by itself protected against ethanol-induced gastric lesions. Our results suggest that mu-receptors are probably not involved in the gastric cytoprotective action of opioids.

Administration, Oral↗