Drugs online research references
Am Heart J. 1982 Aug;104(2 Pt 2):515-20.
Withdrawal of beta-blocking drugs.
Walden RJ, Hernandez J, Yu Y, Al-Khader A, Prichard BN.
Our early observations indicated that when treatment was changed from propranolol to placebo, anginal patients experienced a higher incidence of chest pain during the first week of placebo treatment compared to the second week. Since then, there have been several reports of myocardial infarction and sudden death occurring when propranolol therapy has been stopped. However, more formal hospital studies have indicated that ischemia from propranolol withdrawal is relatively infrequent. Studies in normal subjects and hypertensive patients have shown an increase in beta-receptor sensitivity as suggested by increased responsiveness to isoprenaline after propranolol withdrawal. Some investigators have found an increase in free triiodothyronine levels. Catecholamine levels do not appear to be raised. Other relevant factors in ischemic patients might be a reversal of the favorable rightward shift of the oxyhemoglobin dissociation curve or a reversal of reduced platelet aggregation produced by propranolol. Last, propranolol withdrawal in patients who have received the drug for a considerable period might unmask a withdrawal in patients who have received the drug for a considerable period might unmask a progression of the disease process, so that in the absence of beta blockade oxygen supply is inadequate to meet the requirements of relatively ischemic areas even at rest. Whether all beta blockers are similar to propranolol in this regard is unknown. We are examining, in normal volunteers, the sensitivity of the beta receptor after the withdrawal of atenolol, pindolol, or propranolol, administered for at least 2 weeks after final dose adjustment to levels sufficient to produce maximum inhibition of exercise tachycardia. The sensitivity of the beta receptor is being assessed by the response of bolus injections of isoprenaline and the response to exercise tachycardia.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6125098&dopt=Abstract
Life Sci. 1982 Aug 16;31(7):701-8.
Pharmacological experiments demonstrate that toad (Bufo marinus) atrial beta-adrenoceptors are not identical with mammalian beta 2- or beta 1-adrenoceptors.
O'Donnell SR, Wanstall JC.
Chronotropic responses to sympathomimetic amines of isolated atrial preparations from toads (Bufo marinus) were mediated by beta-adrenoceptors since isoprenaline was more potent than adrenaline and noradrenaline, and propranolol was a potent antagonist (pA2, adrenaline as agonist = 9.33). The beta-adrenoceptors had some of the characteristics of mammalian beta 2-adrenoceptors in that (i) adrenaline was more potent than noradrenaline and (ii) the pA2 values of two selection beta-adrenoceptor antagonists, atenolol (pA2 = 5.84) and alpha-methylpropranolol (pA2 = 8.42), were close to the values reported on beta 2-adrenoceptors in mammalian tissues. However, the relative potencies of adrenaline, isoprenaline, noradrenaline, rimiterol, salbutamol and fenoterol (1 : 45.8 : 0.07 : 3.3 : 1.05 : 0.32) did not correspond to the relative potencies reported for these agonists on mammalian tissues which contain predominantly beta 2-adrenoceptors. Also the pA2 value for the beta 2-selective antagonist, ICI 118,551 (7.89, adrenaline as agonist) was lower than its reported pA2 on beta 2-adrenoceptors in mammalian tissues. There was no evidence that the response was mediated by both beta 1- and beta 2-adrenoceptors since Schild plots for ICI 118,551 using three agonists of differing selectivity (adrenaline, rimiterol and noradrenaline) were superimposed. It is concluded that, although toad atrial beta-adrenoceptors have several characteristics in common with beta 2-adrenoceptors in mammalian tissues, these amphibian beta-adrenoceptors are not identical with mammalian beta 2-adrenoceptors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6127586&dopt=Abstract
Eur J Clin Pharmacol. 1990;38(4):329-34.
Prescription monitoring of drug dosages in the county of Jamtland and Sweden as a whole in 1976, 1982 and 1985.
Wessling A, Boethius G, Sjoqvist F.
National Corporation of Pharmacies, Stockholm.
Prescribed doses of drugs for which individualisation of dosage is deemed necessary were recorded from one national and one local Swedish prescription monitoring study for the years 1976, 1982 and 1985. Dose patterns were analysed in order to determine whether the practice of individualising drug doses had become more widely adopted by physicians. Amongst drugs eliminated primarily by metabolism, (propranolol and amitriptyline were prescribed in highly variable doses (30-fold or more). The three commonest doses of these agents accounted for about 60% of the prescriptions. In general, doses decreased with increasing patient age. Prescribing practices for piroxicam differed markedly from those of propranolol and amitriptyline, with one fixed dose of piroxicam accounting for about 90% of all prescriptions. For drugs eliminated mainly by renal excretion (digoxin, cimetidine and atenolol) there was an 8-10-fold variation in the prescribed doses. The most frequent dose of these drugs accounted for 40-60% of the prescriptions. Doses of cimetidine and atenolol were lowered only in the oldest patients. The doses of digoxin decreased more evenly with increasing age, and were reduced in elderly patients on long-term maintenance therapy. The difference in digoxin dose between young and old patients increased during the study period. Prescription monitoring as a method for following-up drug usage may be instrumental in evaluating the effect of drug educational efforts.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2344856&dopt=Abstract
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