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Bradycardic effect

A QSAR for which the standard error of each descriptor is given concerns the bradycardic effect of a series of tetraalkylbispidines [47]. The QSAR models the selectivity between the desired bradycardic effect and the adverse contractile effect. It is important, in assessing and modeling drug toxicity, that the toxic effect is assessed relative to the desired effect as described above. The QSAR developed for the selectivity of the tetraalkylbispidines was ... [Pg.478]

To mimic melatonin action and increase the half-life is the goal of melatonin receptor agonists, which are the more recent addition to the insomnia therapeutic armamentarium. These compounds, in addition to use for insomnia, may have potential application in the synchronization of disturbed circadian rhythms, sleep disturbances in the elderly, seasonal depression and jet lag, to name a few. Furthermore, studies have shown that melatonin receptor agonists do not induce any of the hypothermic, hypotensive or bradycardic effects caused by melatonin in humans [27,28]. [Pg.68]

The effects of the ergot alkaloids on the central nervous system are very diverse as sites of action are situated in the vasomotor center and the cardiac inhibitory center in the medulla oblongata as well as in the sympathetic structures of the diencephalon, particularly the hypothalamus. The inhibition of the vasomotor center and of tire baroceptive reflexes and the stimulation of the vagal nuclei are resppfisible for the vasodilator, hypotensive, and bradycardic effects, especially in the case of the peptide type of alkaloid. Some also have a stimulating effect on the vomiting center. [Pg.773]

BETA-BLOCKERS MEFLOQUINE t risk of bradycardia Mefloquine can cause cardiac conduction disorders, e.g. bradycardia. Additive bradycardic effect. Single case report of cardiac arrest with co-administration of mefloquine and propanolol, possibly caused by Q-T prolongation Monitor PR closely... [Pg.71]

BETA-BLOCKERS DILTIAZEM t hypotensive and bradycardic effects cases of severe bradycardia and AV block when both drugs are administered concurrently in the presence of pre-existing heart failure or conduction abnormalities Additive effects on conduction diltiazem causes bradycardia, sinoatrial block and AV block. Also, diltiazem inhibits CYP1A2-mediated metabolism of propanolol Monitor PR, BP and ECG at least weekly until stable. Warn patients to report symptoms of hypotension (light-headedness, dizziness on standing, etc.)... [Pg.73]

CALCIUM CHANNEL BLOCKERS ANAESTHETICS -GENERAL, INHALATIONAL t hypotensive effects of dihydropyridines, and hypotensive/bradycardic effects of diltiazem and verapamil Additive hypotensive and negative inotropic effects. General anaesthetics tend to be myocardial depressants and vasodilators they also 1 sinus automaticity and AV conduction Monitor BP and ECG closely... [Pg.78]

Bradycardic effects of -adrenergic receptor agonist Hypertensive effects l l — —... [Pg.243]

In Table 3 the averaged pharmacodynamic parameters for the heart rate of 6 - 7 rats are summarized. For the bradycardic effects the EC5o values (based on free drag concentrations, i.e. not bound to plasma proteins) were equivalent to 1.6 nM, 19 nM, 56 nM and 830 nM for CPA, 5 -deoxyCPA, 3 ->deoxyCPA and 2 -deoxyCPA, respectively. The E values of 2 - and 3 -deoxyCPA were lower than those of the other compounds. EC50 and ECjou were significantly different between the four compounds. [Pg.190]

As early as in the 1970s, the potential use of cannabinoid ligands as antihypertensive agents had been considered (Archer 1974 Crawford and Merritt 1979 Varma et al. 1975 Zaugg and Kyncl 1983), in the hope that their neurobehavioral and cardiovascular effects could be separated. Although an early study in normotensive rats indicated rapidly developing tolerance to the hypotensive and bradycardic effects of THC (Adams et al. 1976), a subsequent study in spontaneously hypertensive rats (SHR) found no evidence for tolerance for the same effects during a similar, 10-day treatment period (Kosersky 1978). [Pg.617]

Heart block is a contraindication for the nondihydropyridines. The most common side effects are bradycardia and heart block (for the nondihydropyridines). Peripheral edema and headache are also common. Nondihydropyridines exacerbate bradycardic effects of /S-blockers, and verapamil raises digoxin serum concentrations by 70%. Diltiazem raises cyclosporine serum concentrations. Intravenous calcium salts inhibit the pharmacologic effect of CCBs. Generic formulations or similar products, but not necessarily generic equivalents to the original brand names, are available for verapamil, nifedipine, and diltiazem. [Pg.364]

Alkylation of clonidine (133) with allyl bromide gave alinidine (138) [167] and with 2-chlorotetrahydropyran piclonidine (139) [168]. Preliminary clinical trials of alinidine demonstrated a bradycardic effect mediated through direct action on the atrial sinus [167], The slow and economic heart rate was thought to be desirable in the management of coronary heart disease [169]. Piclonidine is less potent than clonidine, but it does not evoke hypertensive episodes or cause sedation [168,170,171]. [Pg.230]

It would appear that the bradycardic effects of the beta blockers and the acetylcholine-like effects of these anticholinesterase drugs can be additive. These were inadequately controlled by the use of atropine in some of the instances cited. The myasthenic symptoms may be due to beta blockers exerting a depressant effect on the neuromuscular junction. ... [Pg.835]

The bradycardic effects of the beta blockers can be additive with the delay in conduction through the atrioventricular node caused by diltiazem. This advantageously increases the antianginal effects in most patients, but in a few these effects may exacerbate existing cardiac abnormalities. Diltiazem apparently also inhibits the metabolism of propranolol and metoprolol, but the exact mechanism for this is not clear. ... [Pg.840]

There is no pharmacokinetic interaction between digoxin and tacrine or donepezil. The bradycardic effects of anticholinesterases and digoxin may possibly be additive. [Pg.909]

Phenytoin has a stabilising effect on the myocardial cells so that the toxic threshold of digoxin at which arrhythmias occur is raised. However, the bradycardic effects of the digitalis glycoside are not opposed and the lethal dose is unaltered, so that the cardiac arrest reported would appear to be the result of excessive bradycardia. It seems possible that the fall in plasma digitoxin levels may be due to a phenytoin-induced increase in the metabolism of the digitoxin by the liver. ... [Pg.909]

In 12 healthy subjects bepridil 300 mg daily for a week raised the serum levels of digoxin 375 micrograms daily by 34% (from 0.93 to 1.25 nanograms/mL). Five of them had mild to moderate headache, nausea and dizziness for 1 to 3 days shortly after concurrent use was started. The bradycardic effects of the two drugs were found to be additive, while the negative inotropic effects of the bepridil and the positive inotropism of the increased serum digoxin levels were almost balanced. ... [Pg.914]

Beta-blockers may have enhanced bradycardic effects. [Pg.339]


See other pages where Bradycardic effect is mentioned: [Pg.126]    [Pg.402]    [Pg.33]    [Pg.137]    [Pg.566]    [Pg.109]    [Pg.68]    [Pg.402]    [Pg.371]    [Pg.3256]    [Pg.603]    [Pg.615]    [Pg.237]    [Pg.46]    [Pg.846]    [Pg.884]    [Pg.909]    [Pg.297]   
See also in sourсe #XX -- [ Pg.478 ]




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Bradycardic effects of clonidine

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