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Biomedical subjects

J N Sinha

Publications and source records attributed to J N Sinha.

At least 19 recordsLinked to original sources
PubMed1997

Evidence for antiaggressive property of some calcium channel blockers.

The effect of calcium channel blockers on foot shock induced (aggression (FSA) were studied in mice. Verapamil, (10, 20 and 40 mg kg-1 i.p.) diltiazem (20 and 40 mg kg-1 i.p.) and nifedipine (25 and 50 mg kg-1 i.p.) significantly reduced fighting episodes. Diltiazem and nifedipine blocked the amphetamine induced facilitation of FSA, while verapamil blocked both amphetamine as well as physostigmine induced facilitation of FSA. These findings suggest that calcium channel blockers possess antiaggressive activity, which may be attributed to decrease in central dopaminergic and/or cholinergic mechanism.

Aggression↗
PubMed1991

Protection against gastric ulcer by verapamil.

The effect of verapamil, a calcium channel blocker, was studied against stress (cold restraint), aspirin and pylorus ligation induced gastric ulcers in rats. Verapamil inhibited ulcerogenic response and ulcer index in all the three types of ulcers. Verapamil also decreased total and free gastric acidity without changing gastric secretory volume.

Animals↗
PubMed1991

Evidence for a central component in the cardiovascular effects of calcium channel blockers.

The possibility of a central component in the cardiovascular effects of peripherally administered calcium channel blockers has been explored through a comparison of the effects observed after intravenous (i.v.) and intracisternal (i.c.) administration of verapamil and diltiazem in chloralose-anesthetized and artificially ventilated cats. Both agents produced relatively greater effects after i.c. than after i.v. administration. The bradycardiac effect following i.c. as well as i.v. administration was totally abolished by bilateral cervical vagotomy, and the hypotensive effect was attenuated by this procedure. The results strongly suggest the existence of a central component in the cardiovascular effects of both agents.

Animals↗
PubMed1990

Opioid and non-opioid central cardiovascular effects of ketamine.

The cardiovascular responses to ketamine injected intracisternally were examined in chloralose anaesthetized cats. Blood pressure and heart rate were recorded at different time intervals after intracisternal injection of drug or saline vehicle. The low doses of ketamine (0.5 or 1.0 mg) elicited dose dependent increase in blood pressure and heart rate. In contrast the high dose of ketamine (4 mg), produced a fall in blood pressure and heart rate. The cardiovascular response elicited by the low dose was naloxone insensitive and completely blocked by haloperidol, but not by dopamine antagonist pimozide. The vasodepressor and bradycardiac effect of the 4 mg dose was naloxone antagonizable. These data show that excitatory cardiovascular effects of the low dose result from a naloxone resistant site while in high doses an inhibitory effect is elicited by action at naloxone sensitive opiate receptors.

Animals↗
PubMed1989

Central alpha-adrenoceptor influence over the cardiovascular reflexes activated by veratrine.

Intravenous veratrine induced alterations in cardiovascular parameters in cats were used as a tool for assessing the influence of central alpha-adrenoceptors over reflex adjustments in the heart rate and blood pressure. Blockade of central alpha 2-adrenoceptors with idazoxan or yohimbine, inhibited, while their activation by clonidine, as also blockade of alpha 1-adrenoceptors, with prazosin, potentiated the veratrine induced bradycardia. The hypotensive effect was relatively unaltered by these treatments. Low doses of clonidine potentiated the veratrine-induced bradycardia. It appears that alpha 2-adrenoceptor mechanisms exert greater control over the reflex regulation of heart rate than over reflex control of blood pressure.

Animals↗
PubMed1986

Sulphinpyrazone and the platelet serotoninergic mechanism in ischaemic heart disease.

A double blind study in 25 patients with ischaemic heart disease and 20 matched healthy controls examined the effect of sulphinpyrazone on the uptake of serotonin by platelets and the basal concentrations of serotonin in platelets. Uptake was measured using tritium labelled serotonin and basal concentrations estimated spectrophotofluorometrically. Serotonin uptake was significantly increased both in the patients with chronic stable angina of effort and in those with a history of myocardial infarction six months or more previously. Sulphinpyrazone reduced serotonin uptake from 94.25 (SE 8.65) to 57.86 (5.37) cpm/10(8) platelets after 24 weeks of treatment in the group with stable angina and from 137.45 (16.26) to 68.08 (8.38) cpm/10(8) platelets in the myocardial infarction group. Raised basal concentrations in the two groups were also reduced by sulphinpyrazone. Placebo had no effect on serotonin uptake or basal concentrations in either group of patients. The ability of sulphinpyrazone to inhibit uptake and reduce basal concentrations of serotonin in patients with ischaemic heart disease may be yet another mechanism through which this drug exerts its beneficial antiplatelet effect.

Adult↗
PubMed1986

Role of medullary cholinoceptors in baroreflex bradycardia.

Cholinergic receptors present in three medullary nuclei namely, the nucleus tractus solitarii (NTS), nucleus ambiguous (AMB) and the dorsal motor nucleus of the vagus nerve (DMV) have been studied with regard to their role in regulation of heart rate (HR), blood pressure (BP) and baroreceptor reflex activation induced bradycardia in cats. Microinjection of carbachol into NTS was without effect while administration of carbachol or pilocarpine into AMB and DMV elicited dose related decrease in HR without affecting BP. These effects were completely antagonized by ethylbenztropine. Bilateral muscarinic cholinoceptor blockade of either AMB or DMV, with ethylbenztropine, produced a partial inhibition of the baroreflex bradycardia while intracisternal ethylbenztropine completely abolished this reflex response. Involvement of muscarinic cholinoceptors of AMB or DMV in baroreflex mediated adjustments of HR is therefore suggested.

Animals↗
PubMed1985

An analysis of the alpha-adrenoceptor modulation of vasomotor tone at the level of lateral medullary pressor area (LMPA).

Microinjection of noradrenaline and clonidine into lateral medullary pressor area (LMPA) of chloralose anaesthetized cats produced dose dependent decrease in blood pressure without affecting heart rate, while phenylephrine did not elicit any cardiovascular response. Selective alpha 2-adrenoceptor antagonists idazoxan and piperoxan, microinjected locally, blocked the effects of the agonists but prazosin and phenoxybenzamine, which are relatively selective for alpha 1-adrenoceptors, failed to do so. Clonidine did not elicit any response in guanethidine pretreated cats but noradrenaline microinjected into LMPA of these animals induced a pressor response which was blocked by prazosin pretreatment. It is concluded that catecholaminergic fibres impinging upon this area inhibit the activity of the inhibitory second order baroreceptor neurone by activating alpha 1-adrenoceptors while alpha 2-adrenoceptors situated presynaptically on these inhibitory catecholaminergic nerve terminals are responsible for the manifestation of the hypotensive effect of clonidine and exogenously administered noradrenaline.

Adrenergic alpha-Agonists↗
PubMed1984

An investigation into the mechanism of cardiovascular responses elicited by electrical stimulation of locus coeruleus and subcoeruleus in the cat.

Electrical stimulation of locus coeruleus (LC) and subcoeruleus (SC) elicited an increase in heart rate (HR) and blood pressure (BP). Adrenergic neurone blockade in the posterior hypothalamus with guanethidine and also bilateral adrenalectomy completely blocked the LC stimulation induced cardiovascular responses. The cardiovascular responses elicited by electrical stimulation of SC were, however, unaffected by the former and only partially inhibited by the latter. It is suggested that the LC stimulation-evoked rise in HR and BP is mediated by catecholamine release from the adrenal medulla due to an activation of the hypothalamic-adrenal axis. The cardiovascular responses elicited by stimulation of SC are mainly due to activation of the sympathetic preganglionic neurones and are further augmented by the adrenal catecholamine release.

Adrenal Medulla↗
PubMed1984

Nucleus locus coeruleus: evidence for alpha 1-adrenoceptor mediated hypotension in the cat.

Microinjection of noradrenaline or phenylephrine into the nucleus locus coeruleus of cats induced a dose dependent and long lasting hypotension. Clonidine was required in a dose of 1 microgram for eliciting a significant hypotension while its lower doses (up to 500 ng) failed to elicit any significant cardiovascular alteration. The effects on heart rate evoked by these agents were insignificant. Microinjection of alpha-adrenoceptor antagonists prazosin, piperoxan and RX 781094 per se did not evoke any significant cardiovascular effects and only prazosin pretreatment showed dose dependent antagonism of the hypotensive effect of clonidine. Piperoxan was required in four times higher dose (20 micrograms) to partially antagonize the clonidine induced hypotension. RX 781094, a selective alpha 2-adrenoceptor antagonist, however, even up to a dose of 20 micrograms (four times that of prazosin) did not alter the effect of clonidine. Similar pattern of antagonism was also seen for noradrenaline and phenylephrine. The results demonstrate the presence of alpha 1-adrenoceptors in the nucleus locus coeruleus, the activation of which leads to a fall in blood pressure.

Adrenergic alpha-Antagonists↗
PubMed1984

Anti-inflammatory activity of amino acyl benzoates.

Nineteen new piperazino or morpholino amino acyl benzoates were synthesized and screened against carrageenin induced oedema in albino rats. Several compounds of the series showed potent anti-inflammatory activity. Compound 10 was found to be the most potent. This compound was further evaluated in detail and compared with phenylbutazone for its relative anti-inflammatory potency and ulcerogenic liability. The compound, in addition, was compared with acetyl salicylic acid for its analgesic activity. This compound showed potent ant-inflammatory activity with minimal ulcerogenic liability.

Aminobenzoates↗
PubMed1984

Spinal site of antiarrhythmic action of morphine and pethidine in normal and spinal cord transected dogs.

In coronary artery ligated conscious dogs, intravenous (i.v.) injection of both morphine (8.0 mg/kg) and pethidine (12.0 and 24.0 mg/kg) inhibited the cardiac arrhythmia while naloxone (1.0 mg/kg) facilitated it. Intravenous pretreatment with naloxone completely blocked the morphine induced inhibition of the arrhythmia. Pethidine, however, elicited significant inhibition of the arrhythmia in the naloxone pretreated animals but its duration of action was markedly reduced. The temporal effect of i.v. injection of xylocaine (24.0 mg/kg) was parallel to that of pethidine (24.0 mg/kg) injected i.v. in the naloxone pretreated animals. In cervical spinal cord transected and bilaterally vagotomized dogs, i.v. injection of only 50.0 micrograms/kg of morphine elicited significant inhibition of the arrhythmia which was completely blocked by intrathecal pretreatment with a small dose (1.0 micrograms/kg) of naloxone. The same dose of naloxone, when given intravenously, failed to block the effect of morphine. The antiarrhythmic activity of morphine against the cardiac arrhythmia induced by coronary artery ligation appears to be due to activation of spinal opioid receptors. The local anaesthetic activity of pethidine contributes towards its early phase of antiarrhythmic activity.

Animals↗
PubMed1983

Evidence for involvement of alpha 2-adrenoceptors in the nucleus ambiguous in baroreflex-mediated bradycardia.

Microinjection of noradrenaline and clonidine into the nucleus ambiguus elicited dose-dependent bradycardia with insignificant alteration of blood pressure. Phenylephrine failed to elicit any cardiovascular effect. The bradycardic effects of noradrenaline and clonidine were antagonized by piperoxan but not by phenoxybenzamine. Adrenergic neurone blockade with local guanethidine pretreatment also abolished the response to clonidine. No significant cardiovascular effect of clonidine microinjection into the nucleus ambiguus was observed in bilaterally vagotomized animals. The baroreflex bradycardia induced by volume loading as abolished by yohimbine and piperoxan but not by phenoxybenzamine, microinjected bilaterally into the nucleus ambiguus. These results demonstrate the presence of cardioinhibitory, presynaptic alpha 2-adrenoceptors in the nucleus ambiguus and their involvement in baroreflex bradycardia.

Adrenergic alpha-Agonists↗
PubMed1983

Effects of morphine and pethidine on coronary vascular resistance, blood pressure, and myocardial infarction-induced cardiac arrhythmias.

In the present study, the effects of morphine and pethidine on coronary vessel resistance (CPP), blood pressure (BP), and experimental myocardial infarction-induced cardiac arrhythmia were investigated. Both morphine and pethidine induced a fall in CPP and BP and inhibited the cardiac arrhythmia. The morphine effects on CPP and BP were largely blocked by mepyramine. The effects of pethidine, on the other hand, were not blocked by mepyramine, propranolol, or atropine. An interesting dose dependent inhibition of cardiac arrhythmia was observed with pethidine.

Animals↗