Kafiluddi R, Kennedy R H, Seifen E
Department of Pharmacology and Interdisciplinary Toxicology, University of Arkansas for Medical Sciences, Little Rock.
J Pharmacol Exp Ther. 1988 Feb;244(2):556-63.
This study was designed to examine effects of theophylline, a methylxanthine, on both the positive inotropic and toxic actions of cardiotonic steroids in cardiac muscle isolated from guinea pig heart. In electrically paced left atrial muscle, 0.3 mM theophylline reduced both the maximum developed tension observed in the presence of increasing concentrations of strophanthidin and the dose of this steroid that first elicited extrasystoles. Similarly, 0.3 mM theophylline decreased the time to onset of arrhythmias produced by 5 microM digoxin and the fractional occupancy of specific binding sites on Na,K-adenosine triphosphatase by digoxin at the onset of these dysrhythmic events. A higher level of theophylline (6.5 mM) severely diminished or prevented the positive inotropic and arrhythmogenic actions of cardiotonic steroids while promoting the contracture elicited by these digitalis-like compounds. In spite of the severe contracture observed in the presence of 6.5 mM theophylline plus 5 microM digoxin, the digoxin fractional occupancy was significantly less than that observed at the onset of digoxin-induced extrasystoles and contracture in the absence of theophylline. In radiolabeled ligand binding experiments, 6.5 mM theophylline reduced the affinity of specific binding sites for ouabain while having no effect on receptor density. These results, when considered in light of previous reports by other investigators, suggest that moderate concentrations of methylxanthines promote cardiotonic steroid-induced arrhythmias by increasing Ca++ influx and its uptake into sarcoplasmic reticulum. Higher levels seem to antagonize the arrhythmogenic actions by inhibition of sarcoplasmic reticular Ca++ uptake and by antagonism of receptor binding.
本研究旨在考察甲基黄嘌呤类药物茶碱对豚鼠心脏分离出的心肌中强心苷类药物的正性肌力作用和毒性作用的影响。在电刺激的左心房肌中,0.3 mM茶碱可降低在毒毛花苷浓度增加时观察到的最大收缩张力,以及首次引发期前收缩的该类甾体药物剂量。同样,0.3 mM茶碱可缩短5 microM地高辛诱发心律失常的起始时间,并降低心律失常发生时地高辛对钠钾-ATP酶特异性结合位点的占有率。更高浓度的茶碱(6.5 mM)可严重减弱或阻止强心苷类药物的正性肌力作用和致心律失常作用,同时促进这些洋地黄样化合物诱发的挛缩。尽管在6.5 mM茶碱加5 microM地高辛存在时观察到严重挛缩,但地高辛占有率显著低于在无茶碱情况下地高辛诱发期前收缩和挛缩起始时的占有率。在放射性标记配体结合实验中,6.5 mM茶碱降低了哇巴因特异性结合位点的亲和力,而对受体密度无影响。结合其他研究者之前的报告来看,这些结果表明,中等浓度的甲基黄嘌呤类药物通过增加Ca++内流及其向肌浆网的摄取来促进强心苷类药物诱发的心律失常。更高浓度似乎通过抑制肌浆网Ca++摄取和拮抗受体结合来拮抗致心律失常作用。