Drugs online research references
Pacing Clin Electrophysiol. 1984 Jul;7(4):622-7.
Treatment of life-threatening ventricular arrhythmias by a combination of antiarrhythmic drugs and right ventricular pacing.
Ector H, Van Brabandt H, De Geest H.
Thirteen patients with intractable ventricular arrhythmias were studied; they underwent long-term treatment by a combination of antiarrhythmic drugs and ventricular pacing. Eleven patients had a history of tachycardia and two had torsade de pointes; eleven of thirteen had had cardioversion and/or defibrillation. Prior to permanent pacemaker implantation, temporary pacing in the VVI mode was used in combination with one or more of the following drugs: amiodarone, aprindine, digitalis, metoprolol, mexiletine, procainamide, pindolol, propranolol, or quinidine. Various pacing rates were tried; when permanent pacing was instituted, a unipolar system which was at least rate-programmable was used. Right ventricular VVI pacing, combined with drug therapy, was successful in ten of thirteen patients. Five of the ten patients are alive and free of arrhythmias after 78, 72, 72, 54, and 11 months, respectively. Although five patients died (after 60, 48, 30, 24, and 9 months, respectively), none of the deaths were related to arrhythmias. We suggest that in patients with ventricular arrhythmias refractory to conventional treatment, a therapeutic trial of right ventricular VVI pacing in combination with a drug regimen be used.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6205361&dopt=Abstract
J Pharmacol Exp Ther. 1986 Jul;238(1):378-87.
Antihypertensive effects of 12 beta adrenoceptor antagonists in conscious spontaneously hypertensive rats: relationship to changes in plasma renin activity, heart rate and sympathetic nerve function.
Antonaccio MJ, High J, DeForrest JM, Sybertz E.
Twelve beta adrenoceptor antagonists were examined for their effects on mean blood pressure (MBP), heart rate (HR), plasma renin activity (PRA) and sympathetic nerve function in spontaneously hypertensive rats (SHR). The selected drugs included cardioselective agents (acebutolol, atenolol and metoprolol), agents with intrinsic sympathomimetic activity (oxprenolol, acebutolol, alprenolol and pindolol) and agents with local anesthetic activity (propranolol, oxprenolol, acebutolol, alprenolol and labetalol). All 12 beta adrenoceptor antagonists, administered once daily for 4 days (30 mg/kg p.o.), significantly decreased MBP of SHR. This reduction in MBP was dissociable from both reductions in HR as well as peripheral beta adrenoceptor blockade. In addition, the onset of MBP reduction was slower than the onset of beta adrenoceptor blockade and became greater with duration of treatment. PRA activity was significantly and markedly reduced by both bunolol and metoprolol shortly after dosing at a time when HR was significantly reduced but MBP was not. Conversely, at a time when MBP was significantly reduced by both bunolol and metoprolol, PRA and HR were found to be normal. The changes in HR and PRA were correlated with peripheral beta adrenoceptor blockade but changes in MBP were not. Bunolol, metoprolol and propranolol had no consistent inhibitory effect on pressor responses to nerve stimulation in pithed SHR, although positive chronotropic responses to norepinephrine, tyramine, dimethylphenylpiperazinium and angiotensin I and II were significantly and markedly reduced. It is concluded that beta adrenoceptor antagonists, as a class, reduce MBP of conscious SHR, provided that sufficient time is allowed for this observation to occur. Furthermore, the reduction in MBP caused by beta adrenoceptor antagonists is unrelated to acute beta adrenoceptor blockade, changes in HR, reductions in PRA or inhibition of sympathetic nerve function. Finally, cardioselectivity, intrinsic sympathomimetric activity and local anesthetic activity are not required for the antihypertensive activity of these agents.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2873238&dopt=Abstract
Hum Toxicol. 1989 Jan;8(1):39-43.
Metoprolol alpha-hydroxylation polymorphism in the San Bushmen of southern Africa.
Sommers DK, Moncrieff J, Avenant J.
Department of Pharmacology, University of Pretoria, South Africa.
1. The metabolic oxidation of metoprolol has been studied in a group of 98 San Bushmen. 2. The amounts of metoprolol and alpha-hydroxy metoprolol excreted in 0-8 h urine collection, after dosing with 100 mg metoprolol, were measured and the metabolic ratio (% dose excreted as metoprolol/% dose excreted as alpha-hydroxy metoprolol) calculated. 3. Frequency distribution and probit plots of the metabolic rate data showed a bimodal distribution with 4.1% of the population exhibiting slow metabolism with an MR greater than 10. 4. These results are much less than found in Caucasians (8.4%) but very different from the unimodal distribution found for Nigerians. 5. A previous study in the same group of Bushmen had revealed that 18 of 96 subjects were poor or non-metabolizers of debrisoquine to 4-hydroxy debrisoquine, but only one of the poor metoprolol metabolizers was a poor metabolizer of debrisoquine. 6. On the basis of these results, the claim of debrisoquine type of polymorphism for beta-adrenoceptor antagonists found in Caucasians cannot be extrapolated to the San Bushmen, and one must query the use of debrisoquine as measure of oxidative status in any group other than Caucasians.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2714809&dopt=Abstract
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