Drugs online research references
J Cardiovasc Pharmacol. 1994 Jan;23(1):66-71.
Negative inotropic effect of propranolol is attenuated in underperfused feline heart with an acute ischemic region.
Birkeland S, Westby J, Hexeberg E.
Department of Surgery, University of Bergen, Haukeland Hospital, Norway.
beta-Adrenergic blockade alleviates myocardial ischemia, probably largely through heart rate (HR) reduction. We hypothesized that the negative inotropic effect of beta-blockade, which is believed to be potentially dangerous, is attenuated in underperfused hearts with an acute coronary artery occlusion. We studied the effect of intravenous propranolol (1 mg/kg i.v.) in feline hearts with acute circumflex coronary artery (LCX) occlusion by cross-oriented segments in normally perfused and mildly underperfused left ventricular (LV) anterior wall. A control group (n = 10) was compared with a stenosis group (n = 9) in which the mean coronary perfusion pressure was reduced (91 +/- 4 g vs. 136 +/- 5 mm Hg, p < 0.01). End-systolic pressure-length (ESP-ESL) relations during dynamic afterload increase and preload reduction were calculated to evaluate regional inotropy. HR and LV peak systolic blood pressure (LVSP) decreased in both groups after beta-blockade (p < 0.05). Subendocardial and mid-myocardial blood flow measured by radiolabeled microspheres decreased in the control group (p < 0.05) but was unchanged in the stenosis group. Systolic shortening of circumferential segments also decreased in the control group (p < 0.05) but was unchanged in the stenosis group. ESP-ESL relations of circumferential segments shifted markedly rightward in the control group, whereas a modest rightward shift was noted in the stenosis group. This study in feline heart with acute LCX occlusion showed an attenuated negative inotropic effect of beta-blockade in underperfused LV anterior wall.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7511737&dopt=Abstract
Indian J Biochem Biophys. 1993 Dec;30(6):389-94.
Is asparagine-linked protein glycosylation an obligatory requirement for angiogenesis?
Banerjee DK, Vendrell-Ramos M.
Department of Biochemistry, School of Medicine, University of Puerto Rico, San Juan 00936-5067.
Dependence of protein N-glycosylation on capillary endothelial cell proliferation has been studied. Amphomycin, a potent N-glycosylation inhibitor, inhibited capillary endothelial cell proliferation in a dose-dependent manner. beta-Agonist isoproterenol as well as other intracellular cAMP enhancing agents, viz. cholera toxin, prostaglandin E1 and 8Br-cAMP, also enhanced capillary endothelial cell proliferation. In addition to cell proliferation, isoproterenol also enhanced protein glycosylation in these cells. Isoproterenol effect was mediated by beta-adrenoreceptors, as it got reduced on pre-treatment of cells with either atenolol or ICI 118, 551 or propranolol. Furthermore, isoproterenol stimulation of protein glycosylation by exogenous dolichyl monophosphate and its inhibition by tunicamycin (GlcNAc-1P transferase inhibitor) supported the concept that isoproterenol specifically stimulated protein N-glycosylation event(s) in the cell.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7516308&dopt=Abstract
Eur J Pharmacol. 1994 Apr 1;255(1-3):99-109.
Effect of interventions that increase cyclic AMP levels on susceptibility to ventricular fibrillation in unanesthetized dogs.
Avendano CE, Billman GE.
Department of Physiology, Ohio State University, Columbus 43210.
Although the autonomic nervous system has been implicated in the formation of ventricular fibrillation, the precise mechanism by which this is mediated remains undetermined. In particular, the role of second messengers, generated by beta-adrenoceptor activation, has been postulated to mediate the pro-arrhythmic effects of the sympathetic nervous system. Thus, a 2 min occlusion of the left circumflex coronary artery was initiated during the last minute of exercise in canines with healed myocardial infarctions (produced by ligation of left anterior descending artery). Fifteen dogs were found to be susceptible to the formation of ventricular fibrillation while 17 animals were resistant. Nine resistant dogs were treated with the phosphodiesterase inhibitor isobutylmethyl xanthine (IBMX, 1 mg/kg) in combination with an infusion of 8-bromo-cAMP (100-150 micrograms/kg/min beginning 45 min prior to exercise). Heart rate and left ventricular dP/dtmax significantly increased, but failed to elicit, arrhythmias during the exercise and ischemia test. Nine resistant animals were also treated with the adenylate cyclase activator forskolin, (100 micrograms/kg), which provoked the same hemodynamic changes as the cyclic AMP infusion but also failed to induce ventricular fibrillation. Both forskolin (n = 3) and IBMX (n = 3) induced large increases in myocardial cAMP levels (control 5.2 +/- 0.5, forskolin 8.1 +/- 0.8 pmol/mg non-collagen protein; control 5.0 +/- 0.8, IBMX 6.8 +/- 0.3 pmol/mg non-collagen protein). Ten resistant animals were treated with the beta-adrenoceptor agonist isoproterenol (1-10 micrograms/kg/min), which failed to cause ventricular fibrillation despite significant increases in the hemodynamic parameters described above. Finally, experiments were repeated after 8-bromo-cAMP infusion and IBMX pretreatment in 8 susceptible animals with pharmacologic denervation (atropine+propranolol+prazosin). In spite of hemodynamic increases indicative of an increase in myocardial cyclic AMP levels, arrhythmias were not re-introduced. These data suggest that changes in cAMP may not be responsible for ventricular fibrillation in this model of sudden cardiac death.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7517886&dopt=Abstract
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