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Biomedical subjects

V K Bhargava

Publications and source records attributed to V K Bhargava.

16 recordsLinked to original sources
PubMed1998

Effect of nimodipine on the efficacy of commonly used antiepileptic drugs in rats.

Effect of nimodipine was studied alone and in combination with phenytoin and valproate in maximal electroshock seizures in rats. The test drug was injected i.p. and seizures elicited by a 60 Hz alternating current of 150 mA intensity for 0.25 sec duration through corneal electrodes. The median effective dose (ED50) of phenytoin, valproate and nimodipine were found to be 13, 255 and 4 mg/kg respectively. Addition of ED50 of nimodipine to ED50 of phenytoin and valproate produced an additive effect. Addition of ED25 of nimodipine to ED25 of phenytoin and valproate produced asynergistic effect. Our results show that addition of nimodipine significantly potentiates the anticonvulsant efficacy of phenytoin and valproate.

Animals↗
PubMed1981

Modification by strychnine and D-tubocurarine of cardiac vagal inhibition in dogs.

Intravenous infusion of strychnine or D-tubocurarine chloride attenuated the cardiac depressant action and fall in blood pressure produced by electrical stimulation of the right vagus nerve in dogs anesthesized with pentobarbitone sodium. The effects of exogenous acetylcholine on the heart and blood pressure (B.P.) were not modified by strychnine or D-turbocurarine. Physostigmine sulphate potentiated the effects of injected acetylcholine without modifying the effects of strychnine and D-tubocurarine on vagal transmission. Dimethylphenylpiperazinium bromide also produced its characteristic effects on the heart and B.P. in the presence of strychnine and D-tubocurarine. The results indicate that strychnine and D-tubocurarine inhibition of vagal transmission is not a result of blockade of peripheral cholinergic receptors or cardiac vagal ganglia. This inhibition occurs presumably via a preganglionic presynaptic action.

Acetylcholine↗
PubMed1981

Effect of some cholinergic drugs on the conditioned pole jump response in rats.

Rats were trained to pole jump to a buzzer as the conditioned response. Cholinergic agents, oxotremorine and physostigmine significantly depressed this response. The effect was blocked by atropine. Nicotine and carbachol failed to modify the conditioned pole jump response. It is suggested that the central muscarinic inhibitory receptors are involved in the action of these drugs.

Animals↗
PubMed1970

Long-lasting convulsant effect on the cerebral cortex of Naja naja venom.

1. A neurotoxic fraction has been prepared from Indian cobra venom (Naja naja) by column chromatography on CM Sephadex.2. When assayed for lethality in mice, or for neuromuscular blocking potency in the rat phrenic nerve-diaphragm preparation, this fraction was 2.4-2.9 times as potent as whole venom.3. Application of either whole venom (0.5-1.0 mg/ml) or the neurotoxic fraction (0.25-1.0 mg/ml) to the exposed cerebral cortex of the rat led to the appearance in the somatosensory evoked potential of abnormal negative waves, resembling in amplitude and latency those produced by the cortical application of strychnine or curare.4. This effect differed from that produced by strychnine or curare in that after washing off the toxin the abnormal responses persisted for as long as the experiment continued (8-9 hours).

Animals↗
PubMed1969

The strychnine-like action of curare and related compounds on the somatosensory evoked response of the rat cortex.

1. Drugs were applied to the cerebral cortex of rats anaesthetized with pentobarbitone and changes measured in the somatosensory primary evoked response.2. Computer-derived averages of thirty-two consecutive responses yielded stable and consistent measurements of the potential changes comprising the evoked response, and comparable records from the opposite (non-drug treated) cortex provided an essential control for systemic actions of the drug.3. The modifications produced by curare and strychnine were indistinguishable. The first positive wave (peak latency 7 msec) was unaltered; the second positive wave (peak latency 11.5 msec) was variably enhanced, and the first and second negative waves (peak latencies 16 and 40 msec) were replaced by a much larger negative wave (peak latency 22 msec).4. The time of onset of the effect on the negative waves and the maximal amplitude attained by the abnormal negative wave were related to the log concentration of the drug used. Curare is approximately 10 times more potent than strychnine.5. Toxiferine I, di-allylnortoxiferine and atropine also produced this effect but were less potent than strychnine.6. Succinylcholine, dihydro-beta-erythroidine and gallamine triethiodide did not produce this effect (in concentrations up to 10(-3)M).7. The observations are consistent with an action of curare and strychnine on an intracortical cholinergic inhibitory system, but other possibilities including a "non-specific excitatory action" cannot be excluded.

Animals↗