Search PubMed⌕ Search

Biomedical subjects

V K Shukla

Publications and source records attributed to V K Shukla.

At least 127 records · Page 7Linked to original sources
PubMed1988

Single dose kinetics of rifampicin and isoniazid in well-nourished and malnourished patients of tuberculosis.

A single dose kinetics of isoniazid and rifampicin alone, and combination was studied in well-nourished and malnourished patients of tuberculosis. The elimination half-life of isoniazid was significantly increased when administered in combination with rifampicin in well-nourished and malnourished patients, while no significant difference was observed in any of the pharmacokinetic parameters of rifampicin in combination with isoniazid or alone in both groups of patients. Results are discussed on the basis of pharmacokinetic drug interaction.

Acetylation↗
PubMed1988

Plasma dapsone and its metabolite monoacetyldapsone levels in leprotic patients.

Dapsone (DDS) is a drug of choice in the treatment of leprosy. The DDS and MADDS levels and different pharmacokinetic parameters after a single dose of dapsone and at steady state in leprotic patients have been studied. At steady state, all the patients showed plasma DDS and MADDS levels above 0.5 micrograms/ml throughout the 24-h duration. There was no significant difference in the elimination half-lives of DDS and MADDS after a single dose as compared to at steady state, but AUC0-alpha for both DDS and MADDS were significantly increased at steady state. From these results, it could be concluded that 100 mg daily dose is sufficient to maintain plasma therapeutic concentration in leprotic patients in Indian population.

Adult↗
PubMed1988

Pharmacokinetics of aspirin and chloramphenicol in normal and leprotic patients before and after dapsone therapy.

Pharmacokinetics of aspirin and chloramphenicol was studied in 16 normal and 16 patients suffering from leprosy. A significant increase (p less than 0.05) in the elimination half-life of chloramphenicol was observed before and after dapsone treatment in leprotic patients as compared with the normal volunteers, while no significant difference was observed in any of the pharmacokinetic parameters with aspirin.

Adult↗
PubMed1987

Antagonism by naloxone of anti-tremorine effect of bromocriptine in mice.

Effects of the opioid antagonist naloxone (10 mg/kg) and its interaction with anticholinergic (scopolamine) and dopaminergic (bromocriptine) agents against tremorine-induced tremors was studied. Naloxone (10 mg/kg) per se gave significant protection and significantly potentiated the protective effect of scopolamine against tremorine-induced tremors at 5 min only. When naloxone and subeffective dose of bromocriptine (2 mg/kg) were administered simultaneously, instead of protection, an enhancement of tremorogenic activity was seen. Although the exact mechanism of this drug interaction is far from clear, a multireceptor involvement (i.e. opioid, dopaminergic and cholinergic type) in the modulation of tremorine-induced tremors in mice has been speculated.

Animals↗
PubMed1986

Fulminant amebic colitis.

Nine patients with fulminating amebic colitis who were treated surgically from 1975 to 1982 are presented. Only those who had bowel resections with exteriorization of the cut ends survived. The pertinent literature is reviewed briefly.

Adolescent↗
PubMed1986

Anticatatonic effect of clonidine: its interaction with dopaminergic, anticholinergic and GABA-ergic drugs.

Anticatatonic effects of systemic (50 micrograms/kg, i.p.) and intracerebroventricularly (5 micrograms/10 microliters/rat) administered clonidine was studied in rats against perphenazine-induced catatonia. Clonidine was found to possess anticatatonic actions in rats as it significantly blocked perphenazine-induced catatonia. When clonidine was administered simultaneously with dopaminergic (dopamine, bromocriptine), anticholinergic (scopolamine, diphenhydramine) and GABA-ergic (GABA, muscimol) agents there was a potentiation of the anticatatonic effect. However, clonidine-anticholinergic combination showed a better protective response as compared to clonidine-dopaminergic combination. The protective effect of clonidine and its modification by anticholinergic agents has been explained on the basis of direct central adrenergic as well as central anticholinergic actions of clonidine. Although higher dose of GABA-ergic agents was not studied due to toxicity, the combined effect of clonidine and GABA-ergic agents has been explained on neurotransmitter interactions.

Animals↗
PubMed1986

MPTP: a pharmacological tool to study parkinsonism.

MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) is reported to selectively degenerate dopaminergic cells of the zona compacta of the substantia nigra and produce Parkinson's-like symptoms in man and animals. Although the exact mechanism of its neurotoxicity is not well defined, a major metabolite MPP+ may be responsible for the ultimate neuron toxicity. Several classes of drugs useful in Parkinson's disease are effective in reversing MPTP-induced neurotoxicity. Future pharmacological studies on the compound may unlock some of the mysteries of the age old disease, parkinsonism.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1986

Modification by clonidine of harmine-induced tremors in mice: involvement of serotoninergic system.

Clonidine exhibited a dose-dependent protection against harmine-induced tremors in mice. This protective effect was not completely blocked by pretreatment with yohimbine. The serotoninergic (5-HT) agonist quipazine and the uptake inhibitor fluoxetine completely antagonized this effect. On the other hand, the 5-HT antagonist cyproheptadine potentiated the protective effect of sub-effective doses of clonidine. These observations suggest a serotonin-mediated action of clonidine in its antitremor action against harmine-induced tremors.

Alkaloids↗
PubMed1986

Assessment of bio(in)equivalence of deriphyllin-digoxin in human volunteers. II. Evaluation of rabbits as qualitative animal model.

In rabbits, a three way cross-over test was carried out to assess bioavailability of digoxin from commercially available 'Deriphyllin-Digoxin' tablets. The in vitro dissolution test showed that these tablets had low dissolution even at the end of 4 hr. The in vivo tests in rabbits compared bioavailability of digoxin from Deriphyllin-Digoxin tablets with that from Lanoxin tablets and intravenous digoxin injection. The treatments were given in randomized order with a minimum of 14 days wash-out period between the treatments. After the drug administrations, periodic blood samples were collected and plasma digoxin concentrations were analysed using radioimmunoassay. As indicated by the results of in vitro dissolution tests, Deriphyllin-Digoxin tablets showed poor and delayed absorption of digoxin in vivo. A parallel study on comparative bioavailability for the same batches of digoxin tablets was also carried out in human volunteers. The study in human volunteers involved 14 subjects and had a cross-over dosing. The bioavailability results in rabbits were qualitatively similar to human bioquivalence studies. This is the first report showing digoxin bioavailability in rabbits corresponding to that in humans. The importance of the rabbit as a secondary model for bioequivalence testing of digoxin formulations has been emphasized.

Administration, Oral↗
PubMed1986

Yohimbine potentiates the anticataleptic action of clonidine against perphenazine-induced catalepsy in rats.

The modulatory role of clonidine and yohimbine on the perphenazine-induced catalepsy was studied in rats. Perphenazine (5 mg/kg) produced severe catalepsy which lasted for more than 4 hr. Clonidine (50 micrograms/kg), an alpha 2-agonist, pretreatment offered protection against perphenazine-induced catalepsy. On the other hand yohimbine (5 mg/kg), an alpha 2-antagonist, pretreatment not only showed per se protective action but also potentiated the effects of clonidine against perphenazine-induced catalepsy. Yohimbine also potentiated the protective action of quipazine, a serotonin agonist. The protective effect of yohimbine is explained on the basis of its serotoninergic action.

Animals↗
PubMed1986

Assessment of bio(in)equivalence of deriphyllin-digoxin in human volunteers.

Bioavailability of digoxin from the formulations of a fixed dose combination of the glycoside with xanthines was compared with that of "Lanoxin". The in vitro analysis of the fixed dose "Deriphyllin-Digoxin" tablets showed that these tablets had low dissolution even at the end of four hours. The in vivo study had a randomized cross-over design with a 14 days wash-out period. The formulations were administered to 14 healthy adult volunteers and periodic blood samples were collected up to 24 hours. The samples were analyzed for digoxin concentration using radioimmunoassay. Results indicate poor and delayed absorption of digoxin from the fixed dose combination. It is concluded that a multiple dose study with pharmacodynamic assessment, in patients or in volunteers, would be adequate to critically reassess the need for the marketed fixed dose combination.

Adult↗
PubMed1985

Primary carcinoma of the gall bladder: a review of a 16-year period at the University Hospital.

A review of the most relevant clinical data of patients with primary carcinoma of the gall bladder referred to our hospital over a 16-year-period has indicated that this is the third most common and aggressive cancer of the gastrointestinal tract. The disease occurs predominantly in elderly females who often present with extremes of clinical symptoms indicating benign biliary disease on the one hand and incurable malignant disease on the other. Laboratory and roentgenographic data tend to confirm the clinical diagnosis of this almost entirely incurable disease. The overall 5-year survival of the patients with primary carcinoma of the gall bladder is less than 1%; a majority of the patients are dead in less than 6 months.

Adenocarcinoma↗