Drugs online research references
J Pharmacol Methods. 1985 Dec;14(4):249-54.
A new model of ventricular fibrillation induced by isoprenaline and catechol-O-methyl transferase inhibitor at a high perfusion temperature in isolated rat hearts.
Sono K, Akimoto Y, Magaribuchi T, Kurahashi K, Fujiwara M.
Isolated rat hearts were perfused with various concentrations of isoprenaline (0.01-10 mumol/liter) for 30 min at a constant flow rate (6.5 ml/min) at 37-44 degrees C. The occurrence of ventricular fibrillations was isoprenaline concentration dependent and also perfusion temperature dependent in the combined treatment with various concentrations of isoprenaline and high perfusion temperatures. When the hearts were perfused with isoprenaline (1 mumol/liter) in the presence of tropolone (100 mumol/liter) at 40-41 degrees C, the duration of ventricular fibrillations was significantly prolonged, but the incidence of ventricular fibrillations was similar to that produced with isoprenaline (1 mumol/liter) alone. The antiarrhythmic drugs such as quinidine sulfate, lidocaine hydrochloride, dl-propranolol hydrochloride, carteolol hydrochloride, atenolol, dl-verapamil hydrochloride, and diltiazem hydrochloride, given at a concentration of 10 mumol/liter, significantly suppressed the incidence and duration of such ventricular fibrillations. Bretylium tosylate (10 mumol/liter) significantly suppressed the duration of the ventricular fibrillations but not their incidence. These results indicate that ventricular fibrillation induced by combined treatment with a high concentration of isoprenaline and tropolone at a high perfusion temperature in isolated rat hearts is a more useful experimental model of arrhythmia than conventional models.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=4079442&dopt=Abstract
Cardiovasc Res. 1979 Oct;13(10):588-94.
Prophylaxis of ventricular fibrillation after acute experimental coronary occlusion by chronic beta-adrenoceptor blockade with atenolol.
Menken U, Wiegand V, Bucher P, Meesmann W.
Acute occlusions of the left circumflex coronary artery were performed in open-chest dogs. A control group (n = 19) was compared with three groups (total n = 17) pretreated once daily with different doses of the cardioselective beta-blocking drug atenolol (ICI 66 082) given by mouth for 5 days. Only animals without coronary collateral vessels were examined, having a mortality rate of 100% in the control group. Arrhythmias and ventricular fibrillation during the first 30 min after coronary occlusion showed a biphasic distribution in time (phase 1a and 1b). A lower degree of beta-adrenoceptor blockade reduced the incidence of arrhythmias and ventricular fibrillation in phase 1a, but fibrillation occurred in all animals during phase 1b. A higher dose of the beta-blocking drug protected the animals from ventricular fibrillation, and arrhythmias in phase 1a were greatly reduced. At all times the ventricular fibrillation threshold in the group pretreated with atenolol was significantly higher than in the control group. In both groups a significant decrease in ventricular fibrillation threshold was found only during phase 1a. The greater sensitivity of phase 1a arrhythmias to beta-blockade and the lack of a decrease in ventricular fibrillation threshold during phase 1b might indicate differences in the genesis of arrhythmias and fibrillation in phases 1a and 1b.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=519661&dopt=Abstract
J Pharmacol Exp Ther. 1991 Oct;259(1):414-22.
Interactions of flerobuterol, an antidepressant drug candidate, with beta adrenoceptors in the rat brain.
Zini R, Morin D, Martin P, Puech AJ, Tillement JP.
Departement de Pharmacologie, Faculte de Medecine de Paris XII, Creteil, France.
Interactions of dl-flerobuterol with central beta adrenoceptors were investigated. It inhibited the binding of [3H]CGP 12177, a selective beta adrenoceptor ligand, to membranes prepared from rat cerebral cortex, cerebellum, heart and lung. The affinity of dl-flerobuterol was very close in all tissues (Ki approximately 1 microM). In cerebral cortex, binding inhibition of [3H]CGP 12177 was stereospecific, l-flerobuterol (Ki = 483 nM) being 70-fold more potent than d-flerobuterol (Ki = 34 microM). Moreover, dl-flerobuterol (Ki = 926 nM) was 7-fold less potent than isoproterenol (Ki = 140 nM) to displace [3H]CGP 12177 binding, but 5-fold more potent than salbutamol (Ki = 4600 nM). Flerobuterol did not inhibit the radioligand binding to the other receptors at the highest concentration tested, thus leading to a very high beta adrenergic selectivity. Flerobuterol increased the concentration of cyclic AMP in slices of rat cerebral cortex in a dose-dependent manner; this effect was antagonized by atenolol and propranolol. Compared to isoproterenol or norepinephrine, which produced cyclic AMP maximal increases of 380 and 460%, respectively, it showed a weaker activity with a maximal stimulation obtained at 100 microM, corresponding to a cAMP increase of 140% over basal value (100%). These data revealed that flerobuterol possessed a beta adrenergic agonist activity. Moreover, it antagonized competitively the isoproterenol- or norepinephrine-stimulated accumulation of cAMP. At low concentrations of isoproterenol or norepinephrine, the stimulation of adenylate cyclase was only due to the action of flerobuterol, but at higher concentrations, the response of isoproterenol or norepinephrine was competitively blocked by flerobuterol. At 10 microM, isoproterenol surmounted fully this antagonism.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1681091&dopt=Abstract
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