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Biomedical subjects

K S Dixit

Publications and source records attributed to K S Dixit.

At least 19 recordsLinked to original sources
PubMed1999

Evaluation of antiallergic activity (type I hypersensitivity) of Inula racemosa in rats.

Alcoholic extract of root of Inula racemosa, was studied for its antiallergic effect in experimental models of type I hypersensitivity, viz. egg albumin induced passive cutaneous anaphylaxis (PCA) and mast cell degranulation in albino rats. The alcoholic extract was prepared by the process of continuous heat extraction. LD50 of this extract was found to be 2100 +/- 60 mg/kg, i.p. Assessment of protection against egg albumin induced passive cutaneous anaphylaxix by different doses of Inula racemosa was done by giving drug intraperitoneally or orally for seven days or once only. Mast cell degranulation studies were done by using compound 48/80 as degranulation agent with same dosage schedule. Inula racemosa (i.p. as well as p.o.) showed significant protection against egg albumin induced PCA. Protection against compound 48/80 induced mast cell degranulation by alcoholic extract of Inula racemosa (single dose) was similar to that of disodium cromoglycate. The seven days drug treatment schedule showed greater protection than disodium cromoglycate intraperitoneally. The results suggest that Inula racemosa possesses potent antiallergic properties in rats.

Animals↗
PubMed1991

Substituted quinazolones as potent anticonvulsants and enzyme inhibitors.

A series of 6,8-disubstituted 3-[5- [[2-hydroxy-3-[(substituted phenyl)amino]propyl]thio]-1,3,4-thiadizol-2-yl] 2-methyl-4(3)- quinazolinones were synthesized whose structures were confirmed by elemental analyses, IR, NMR and mass spectral studies. All these compounds were evaluated in vivo for anticonvulsant and analgesic activities and in vitro for monoamine oxidase and succinate dehydrogenase enzyme inhibitory activities using rat brain homogenate as a source of enzyme at final concentration of 1 x 10(-4) mol/l. ALD50 values indicated their relatively nontoxic nature.

Analgesics↗
PubMed1989

Role of endogenous opioids and histamine in morphine induced emesis.

The role of opioid and histaminergic system in morphine induced emesis was investigated in dogs. Morphine (25 micrograms, icv) consistently evoked emesis with an average latency of 195 +/- 29 sec which was fully accounted for by an action on the chemoreceptor trigger zone (CTZ) as its ablation rendered animals refractory to vomiting. Intraventricular pretreatment with opioid antagonist naloxone, histamine H1 antagonist mepyramine and H2 antagonists metiamide and cimetidine afforded protection to icv morphine emesis. The CSF histamine concentration was significantly raised 5 min after icv morphine administration. The results suggest that both endogenous opioid and histamine are involved in morphine emesis. Naloxone in high doses (1600 micrograms, icv) elicited emesis which was not blocked by CTZ ablation confirming our earlier report.

Animals↗
PubMed1989

Role of dopaminergic system in opioid-induced cardiovascular responses in dogs.

A study was carried out to determine the involvement of dopaminergic system in opioid-induced cardiovascular responses in the dogs. The study population consisted of 32 mongrel dogs of either sexes. The results show that morphine given in small dose (2 mg/kg I.V.) causes significant fall in blood pressure. The results also show that there is involvement of dopaminergic system in opioid-induced vasomotor responses in dogs. Partial blockade of the parenterally induced hypotensive response of morphine by haloperidol given centrally induced hypotensive responses of morphine by haloperidol given centrally in doses, which are too low to be effective by the peripheral route, strongly favours the involvement of central dopaminergic system in the morphine-induced hypotensive responses. The results also show that the hypotensive response of morphine was almost completely blocked after naloxone pretreatment by central route.

Animals↗
PubMed1981

Enkephalin receptors in the emetic chemoreceptor trigger zone of the dog.

1 The emetic action of Met-enkephalin, morphine and naloxone was studied following their administration into the cerebral ventricles of dogs through chronically implanted cannulae and the effect on the responses of ablating the chemorceptor trigger zone (CTZ) was investigated. The opiate antagonist, naloxone, was used to determine the role of enkephalin receptors in emetic responses.2 Administration of Met-enkephalin (1.0 mug/kg) into the IVth ventricle regularly evoked emesis with an average latency of 35 s. A dose of morphine (2.5 mug/kg) which was five times larger was required for a consistent emetic response when introduced into the lateral cerebral ventricle (i.c.v.) as compared to the dose required by the IVth ventricular route. The latency of emetic responses by the latter route of injection of morphine was shorter. This is in accord with an action of morphine on the emetic CTZ.3 After bilateral ablation of the CTZ, intraventricular injections of Met-enkephalin and morphine failed to produce emesis even when given in doses that were 5 to 10 times the dose which regularly elicited emesis in animals with intact CTZ. The emesis produced in dogs by intraventricular Met-enkephalin and morphine is thus fully accounted for by an action on the CTZ.4 Naloxone (i.c.v.) in doses up to 10.0 mug/kg did not cause emesis. However, higher doses of naloxone elicited dose-dependent emesis in dogs. The 100% emetic dose of naloxone was found to be 160 mug/kg and the latency of emesis was 180 s. Unlike Met-enkephalin and morphine, naloxone continued to elicit emesis in CTZ-ablated animals.5 Pretreatment with intraventricular naloxone (1 to 8 mug/kg) blocked the emetic responses induced by intraventricular Met-enkephalin and morphine but not that to apomorphine. The selective protective action of the opiate antagonist against Met-enkephalin and morphine supports the presence of enkephalin receptors in the emetic CTZ.

Animals↗
PubMed1976

Nature of histamine receptors in the emetic chemoreceptor trigger zone.

1 The protective effects of the intracerebroventicular (i.c.v.) administration of the H1-receptor antagonist, mepyramine and the H2-receptor antagonists, burimamide and metiamide on centrally induced histamine-emesis were studied in unanaesthetized dogs. 2 The PD50 values of intraventricular mepyramine, burimamide and metiamide against the 100% emetic dose of histamine (3.0 mg i.c.v.) were found to be approximately 200 mug, 20 mug and 20 mug respectively. 3 Although burimamide (i.c.v. or i.v.) afforded protection against histamine-induced emesis, there was no protection against intravenous apomorphine-or oral copper sulphate-induced emesis. 4 The results suggest that both H1- and H2-histamine receptors in the emetic chemoreceptor trigger zone of the area postrema are concerned in histamine-induced emesis.

Animals↗
PubMed1971

Role of the chemoreceptor trigger zone in cyclopropane induced emesis in dogs.

Inhalation of cyclopropane in dogs, by the closed circuit method, for a fixed period, produced an emetic response during recovery from anaesthesia. Bilateral surgical ablation of the emetic chemoreceptor trigger zone of the area postrema rendered the dogs refractory to several times (3-6) the threshold emetic dose of cyclopropane.

Anesthetics↗