Drugs online research references
Cesk Farm. 1990 May;39(3):118-21.
[Analysis of the adverse effects of drugs at the cellular and subcellular levels]
[Article in Slovak]
Nosal' R, Drabikova K, Pecivova J, Ondrias K, Jakubovsky J.
Ustav experimentalnej farmakologie Slovenskej akademie vied, Bratislava.
A release of histamine after the lipophilic betablockers exaprolol and propranolol correlates with their capability of displacing the bound membrane Ca2+ and increasing the disorder of phospholipidic membranes of the isolated mast cells. Electron microscopy confirmed intracellular displacement of histamine from granules of mast cells after exaprolol without marked structural changes on the plasmatic membrane. Hydrophilic and selective atenolol, which does not possess a histamine-liberating effect, decreases spontaneous transfer of the intracellular calcium, decreases the disorder of the mast-cell membranes, and together with exaprolol and propranolol inhibits, in dose-dependence way, the gain of extracellular histamine in cells. The inhibitory effect of EDTA, tetrodotoxine and suramine on histamine release after exaprolol explains the non-receptor mechanism of exaprolol effect, which confirms a possibility of induction of adverse effects of blockers of the beta-adrenergic receptor in the development of a bronchospasm.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1698127&dopt=Abstract
J Clin Pharmacol. 1987 Nov;27(11):892-901.
A comparison of the side effects of atenolol and propranolol in the treatment of patients with hypertension.
Fodor JG, Chockalingam A, Drover A, Fifield F, Pauls CJ.
Memorial University of Newfoundland, Faculty of Medicine, St. John's, Canada.
A single-blind study was conducted in 52 hypertensive patients, aged 25 to 68 years, to compare the side effects of an equally effective antihypertensive regimen of propranolol and atenolol. All patients had a history of side effects with beta-blocker therapy. Patients were treated with propranolol 40 to 160 mg bid for 8 weeks, followed by atenolol 50 to 100 mg given once daily for 8 weeks, and then rechallenged with the required dosage of propranolol for 8 weeks. Mean systolic and diastolic blood pressures were controlled during all three treatment phases. Side effects showed a definite trend toward improvement during the atenolol treatment phase. CNS side effects, in particular, showed significantly (P less than .05) reduced severity scores and overall incidence rates during the atenolol treatment phase. In conclusion, this study showed that at equally effective antihypertensive dosages the hydrophilic beta blocker atenolol produced significantly fewer CNS side effects than the lipophilic beta blocker propranolol.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2892865&dopt=Abstract
Cardiovasc Drugs Ther. 1988 Nov;2(4):501-12.
Comparative study of the effects of acebutolol, atenolol, d-propranolol and dl,-propranolol on the alterations in energy metabolism caused by ischemia and reperfusion: a 31P NMR study on the isolated rat heart.
Lavanchy N, Martin J, Rossi A.
Laboratoire de Physiologie Cellulaire Cardiaque (URA CNRS 56), Universite Joseph Fourier, Grenoble, France.
31-P NMR spectroscopy data recorded for the isolated heart were analyzed, in conjunction with functional and biochemical variables, in order to investigate the effect observed for several different beta-adrenoceptor antagonists or the alterations provoked by global partial ischemia (37 degrees C, 24 minutes, 1% residual coronary flow) and reperfusion in the metabolism of the myocardium. During ischemia: intracellular acidosis, adenosine triphosphate (ATP) degradation, and inorganic phosphate (Pi) accumulation were found to be reduced whether the perfusion fluid contained: acebutolol 2.7 x 10(-5) M, atenolol 10(-5) M, d-propranolol 10(-5) M, or dl-propranolol 10(-5) M. On reperfusion metabolic and functional variables were variously affected by the different drugs, except the Pi level which was, in all series, significantly lower compared with control hearts. The adenylate charge and the glycogen stores were protected in the acebutolol, dl-propranolol, and d-propranolol groups. The ATP level was higher than in controls only in the acebutolol and atenolol groups. The intracellular pH recovered to values nonsignificantly different from preischemic values in the acebutolol and dl-propranolol-treated hearts only. The mechanical performance, expressed as the rate-pressure product, was unaltered by the ischemia-reperfusion sequence in the acebutolol and d-propranolol series, while decreasing significantly in controls and in the atenolol group. In dl-propranolol-treated hearts the mechanical activity, which in normoxic conditions was already halved during the effect of the drug, remained at this same level after ischemia. From these observations, it appears that the nonspecific properties of the drugs, as distinct from beta-blockade, play an important part in attenuating the ischemia-induced alteration in myocardial metabolism. Thus, it can be postulated that (1) the metabolic effects of dl-propranolol probably result largely from the reduction of heart work induced by this drug; (2) the maintenance of energy metabolism associated with the preservation of the myocardial activity, as observed in the case of acebutolol and d-propranolol, is possibly a consequence of the existence of a membrane-stabilizing activity.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2908708&dopt=Abstract
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