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Biomedical subjects

N S Parmar

Publications and source records attributed to N S Parmar.

At least 37 records · Page 2Linked to original sources
PubMed1987

Studies on ethanol and/or nicotine induced acute changes in the levels of plasma amino acids and other biochemical parameters of male Wistar rats.

The effects of acute administration of ethanol and nicotine either singly or in combination, have been studied on the plasma amino acids levels and certain biochemical and hematological parameters in the rats. Both ethanol and its combination with nicotine produced significant reduction in the levels of a number of amino acids and the total amino acid pool. Only the levels of taurine and hydroxyproline were increased in the ethanol treated rats, whereas its combination with nicotine resulted in markedly elevated levels of hydroxyproline, ornithine and taurine. These changes were also accompanied by a significant rise in blood glucose, ALT, AST, blood urea and uric acid and a significant reduction in the total protein and triglycerides levels. Nicotine by itself produced less profound effect on the plasma amino acids and other biochemical parameters.

Alanine Transaminase↗
PubMed1986

Anti-inflammatory activity of the flavonoid fraction of khat (Catha edulis Forsk).

The administration of the flavonid fraction, isolated from Khat (Catha edulis Forsk), in a dose of 200 mg/kg orally, produced a significant anti-inflammatory activity against the carrageenan induced paw oedema and cotton pellet granuloma in albino rats. The results were comparable with the standard anti-inflammatory drug oxyphenbutazone.

Animals↗
PubMed1986

Anti-inflammatory activity of Commiphora molmol.

The petroleum ether extract of the oleo-gum resin of Commiphora molmol, at a dose of 500 mg/kg body weight, produced significant inhibition of carrageenan induced inflammation and cotton pellet granuloma. The extract also showed significant antipyretic activity in mice. Further studies on the fractionation of phytoconstituents and their mechanism of action are in progress.

Animals↗
PubMed1986

Anti-inflammatory activity of some Saudi Arabian medicinal plants.

Five plants which have been used for the treatment of rheumatism, arthritis and gout in the traditional medicine of Saudi Arabia, were evaluated for their anti-inflammatory properties. Of these the ethanolic extract of Capparis decidua and the aqueous extract of Capparis spinosa were found to possess significant anti-inflammatory activity against carrageenan induced oedema in rats. These two plants were also tested for their antipyretic and analgesic activity. C. decidua was found to possess significant antipyretic effect. Both of them are devoid of analgesic activity.

Animals↗
PubMed1986

Decrease by naloxone of some electrocardiographic and biochemical changes following endotoxin induced shock in rats.

Administration of endotoxin, a lipopolysaccharide extracted from cell walls of gram negative bacteria, elicited alterations in various metabolic parameters and in the electrocardiogram of rats. Cardiac glycogen and serum glucose were decreased, while serum pyruvate and acid phosphatase levels were increased. There was initial tachycardia followed by significant bradycardia and elevation of the ST segment in the animals with shock. Erythrocyte count, haemoglobin and haematocrit were not changed after shock. Treatment with naloxone caused significant decreases in the metabolic and electrocardiographic changes induced by endotoxin.

Acid Phosphatase↗
PubMed1986

Gastric mucosal damage induced by endotoxin shock and its prevention by naloxone and anti-ulcer drugs in rats.

Administration of endotoxin (20 mg/kg i.p.) produced a moderate degree of gastric mucosal damage in rats. The lesions remained confined to the glandular mucosa and consisted of small punctiform lesions, erosions and petechial hemorrhage. The characteristic feature of these lesions was a typical submucosal ecchymosis in the glandular stomach observed in about 30% of the animals. Pretreatment with ranitidine, pirenzepine, proglumide, sucralfate and naloxone produced varying degrees of protection. The ulcerogenic effect of endotoxin shock is apparently mediated through the release of endorphins.

Animals↗
PubMed1986

Gastric antisecretory, gastric and duodenal anti-ulcer and cytoprotective properties of Ro 22-6923, a synthetic trimethyl prostanoid in rats.

Ro 22-6923, a synthetic trimethyl prostanoid, has been studied for its ability to inhibit gastric secretion and to protect the gastroduodenal mucosa against the injuries caused by pyloric ligation, hypothermic restraint stress, nonsteroidal anti-inflammatory drugs (NSAIDs), reserpine, dimaprit, cysteamine and the cytodestructing agents--80% ethanol, 0.6 M HCl, 0.2 M NaOH, 25% NaCl, aspirin 30 mg in 0.35 M HCl and 100 mM sodium taurocholate in 0.2 M HCl. The results of this study demonstrate that Ro 22-6923 has both prophylactic and curative effects on various experimental models. It produces a dose dependent inhibition of the gastric mucosal damage induced by pyloric ligation, hypothermic restraint stress, NSAIDs, reserpine, dimaprit and cytodestructing agents and that of duodenal ulcers induced by cysteamine. It also produces a dose dependent healing of the acetic acid induced chronic gastric ulcers. These observations suggest that Ro 22-6923 exerts its anti-ulcer effects by its antisecretory, gastric mucosal resistance increasing and cytoprotective activities and that it may be a useful therapeutic agent for the treatment of peptic ulcer disease in humans.

Animals↗
PubMed1986

Evaluation of mastic, a crude drug obtained from Pistacia lentiscus for gastric and duodenal anti-ulcer activity.

The effect of mastic, a concrete resinous exudate obtained from the stem of the tree Pistacia lentiscus, has been studied on experimentally-induced gastric and duodenal ulcers in rats. Mastic at an oral dose of 500 mg/kg produced a significant reduction in the intensity of gastric mucosal damage induced by pyloric ligation, aspirin, phenylbutazone, reserpine and restraint + cold stress. It produced a significant decrease of free acidity in 6-h pylorus-ligated rats and a marked cytoprotective effect against 50% ethanol in rats which could be reversed by prior treatment with indomethacin. The protective effect was not seen when it was given intraperitoneally in phenylbutazone and restraint + cold stress models. The reduction in the intensity of ulceration in cysteamine-induced duodenal ulcers was not found to be statistically significant in mastic-pretreated rats. The results suggest that mild antisecretory and a localized adaptive cytoprotectant action may be responsible for its anti-ulcer activity. These observations support the results of an earlier study on the clinical effectiveness of mastic in the therapy of duodenal ulcer.

Animals↗
PubMed1986

Evaluation of genotoxic potential of khat (Catha edulis) in Swiss albino mice.

Genotoxicity of the methanolic extract of khat (Catha edulis) has been evaluated on the male germ cells using the dominant lethal assay procedure in Swiss albino mice. The extract was administered at a dose of 500 mg/kg orally once daily, for five days. Following this sub-acute dose regimen, the effect of khat was studied during the different stages of spermatogenic cycle on the rate of pregnancy and post-implantation losses. Khat reduced the percent pregnancy rates and increased the mean post-implantation losses in the treated group. The increase was found to be statistically significant in the post-meiotic stages.

Animals↗
PubMed1986

Some central effects of indenolol in experimental animals.

Indenolol, a relatively new beta-adrenergic blocking drug, was tested for its effect on the central nervous system. The parameters included its effects on spontaneous motor activity, conditioned avoidance response (CAR) acquisition, pentobarbitone hypnosis, amphetamine induced motor excitation, analgesic activity and rectal temperature in experimental animals. Indenolol was found to significantly decrease the spontaneous motor activity in mice and CAR acquisition in rats. It potentiated the pentobarbitone induced hypnosis and antagonized amphetamine induced excitatory behaviour in mice. It did not show a marked analgesic effect of its own but potentiated the analgesia induced by the subanalgesic dose of morphine. It also produced a significant hypothermic effect in mice. All the effects except on CAR acquisition were obtained in the dose of 50-75 mg/kg body weight administered intraperitoneally. It enhanced CAR acquisition in the specific dose of 5 mg/kg. These observations indicate that indenolol possesses an anxiolytic effect similar to that reported for propranolol and some other beta-blocking drugs.

Adrenergic beta-Antagonists↗
PubMed1986

Effect of domperidone on experimentally induced gastric ulcers in rats.

The effect of domperidone, a peripheral dopamine receptor antagonist, has been studied in the aspirin, phenylbutazone and reserpine induced gastric ulcers in rats. The gastric anti-ulcer activity of domperidone was evident following a single dose as well as a 5-day pretreatment against all the three ulcerogenic drugs. However, the protection in the five-day pretreatment group was greater than in the single dose pretreatment group. It appears that the gastrokinetic properties of domperidone play a significant role in producing this anti-ulcer effect. The study substantiates the results of the clinical observations on the healing of gastric ulcers and provides a rationale for further clinical studies in that direction. The possible mechanisms of action of this agent are discussed.

Animals↗
PubMed1985

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

The effect of nicotine and caffeine pretreatment by feeding nicotine (2.5 mg %), caffeine (30 mg % base), and their combination (nicotine 2.5 mg % + caffeine 30 mg %) 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 caffeine produced any visibly discernible gastric lesions. Their concurrent administration too, did not produce any gastric mucosal injury. Pretreatment with nicotine, caffeine, and their combination resulted in significant augmentation of gastric ulcers produced by aspirin, phenylbutazone, and reserpine. However, caffeine administration produced a comparatively less profound augmentation of experimentally induced gastric lesions than that produced by nicotine pretreatment. The enhancement of gastric ulcers in the groups pretreated with the combination of nicotine and caffeine followed by one of the drugs 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 on pancreatic bicarbonate secretion and the gastric secretory effect of caffeine may be responsible for the potentiation of the ulcerogenic effects of aspirin, phenylbutazone, and reserpine.

Administration, Oral↗
PubMed1985

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

The effects of nicotine (2.5 mg/100 ml), alcohol (25% v/v) and caffeine (30 mg/100 ml base) and their combination (nicotine, 2.5 mg/100 ml; alcohol, 25% v/v; and caffeine, 30 mg/100 ml base) fed in drinking water ad libitum for 21 days were studied on the gastric mucosal damage induced by aspirin, phenylbutazone and reserpine in rats. When given alone, none of them produced any visibly discernible gastric lesions. Their concurrent administration, however, produced some injury to the gastric mucosa which was far less severe than the lesions induced by any of the ulcerogenic drugs used in this study. Pretreatment with nicotine, alcohol and caffeine and their combination resulted in a significant augmentation of gastric lesions produced by aspirin, phenylbutazone and reserpine. These results establish an association between nicotine, alcohol and caffeine in the pathogenesis of gastric ulcers and also implicate them as modifying factors in the genesis of gastric lesions induced by aspirin, phenylbutazone and reserpine.

Animals↗
PubMed1984

Effect of bromocriptine, a dopamine receptor agonist, on the experimentally induced gastric ulcers in albino rats.

The effect of bromocriptine, a dopamine receptor agonist, has been studied on the aspirin, phenylbutazone and reserpine induced gastric ulcers in rats. A single dose of bromocriptine 4 mg/kg s.c. produced a significant exacerbation of gastric ulcers induced by all the three ulcerogenic drugs, whereas in the same dose administered once daily for 5 consecutive days, it produced a marked protective effect in all the models. A review of the literature shows that different mechanisms may be involved in the opposite effects of acutely and chronically administered bromocriptine observed in this study. The study also points towards a role of dopamine in the pathogenesis of gastroduodenal ulceration.

Animals↗
PubMed1984

The effect of nicotine pretreatment on the gastric mucosal damage induced by aspirin and reserpine in rats.

The effect of nicotine pretreatment by feeding nicotine (5mcg/ml) in drinking water ad libitum for 10 days was studied on the aspirin and reserpine induced gastric mucosal damage in rats. The administration of nicotine resulted in the significant augmentation of aspirin (P less than 0.01) and reserpine (P less than 0.05) induced gastric ulcers. The mechanism(s) involving the sensitization of gastric mucosa towards the ulcerogenic effect of aspirin and reserpine may be responsible for the increased intensity of gastric ulcers in both the groups. The study indicates the possibility of a similar interaction in heavy smokers who ingest these drugs.

Animals↗
PubMed1984

Histidine decarboxylase inhibition: a novel approach towards the development of an effective and safe gastric anti-ulcer drug.

The involvement of histamine in mediating gastric function under normal and pathological conditions has been largely established. The relationship between gastric acid production and peptic ulcer diathesis is also well known. Recently, endogenous histamine formation and its release from mast cells has been implicated in the pathogenesis of human and experimental gastric ulcers produced by restraint and pyloric ligation. It has also been implicated in the gastric mucosal damage produced by drugs like aspirin, phenylbutazone and reserpine. These observations suggest that histidine decarboxylase inhibitors may be useful in the prevention of such lesions. Our studies on the evaluation of some histidine decarboxylase inhibitors show that these compounds have a promising potential for developing an effective and safe anti-ulcer drug. This mini-review incorporates the results of our studies which have been adequately supported by other studies as well.

Animals↗
PubMed1984

The gastric antisecretory activity of 3-methoxy-5,7,3'4'-tetrahydroxyflavan (ME)--a specific histidine decarboxylase inhibitor in rats.

3-Methoxy-5,7,3'4'-tetrahydroxyflavan (ME), a specific histidine decarboxylase inhibitor, has been shown to significantly reduce the gastric acid secretion and gastric tissue histamine levels in 6 h pylorus ligated rats. It has been found to be as effective as cimetidine in reducing the gastric acid secretion. However, cimetidine does not affect the gastric tissues histamine levels in the normal or pylorus ligated rats. These observations clearly establish that the two drugs reduce the gastric acid secretion by different mechanisms and suggest that their combination may show a potentiated gastric anti-ulcer activity.

Animals↗