Abstract
The evidence that free oxygen radicals produced by polymorphonuclear neutrophils (PMN) participate in generation of reperfusion arrhythmias is well documented. The in vitro effect of selected antiarrhythmic drugs on PMN free radicals production was evaluated by luminol- (LuCL) and lucigenin- (LgCL) amplified chemiluminescence stimulated with opsonized zymosan (o.z.) and phorbol myristate acetate (PMA). Fast sodium channel inhibitors varied in the influence on PMN chemiluminescence: from an inhibition in all models studied by procainamide, to lack of an effect by mexiletine. Propafenone, similarly to ajmaline and verapamil, inhibited LuCL stimulated with PMA, as well as LgCL after stimulation with both PMA and o.z. Bretylium tosylate decreased LuCL stimulated with both inducers, with no effect on LgCL. Amiodarone in high concentrations inhibited both LuCL and LgCL. beta-blockers propranolol and practolol impaired LuCL stimulated with o.z., as well as LgCL induced with PMA, whereas alpha-blocker phentolamine inhibited LuCL and LgCL stimulated with both inducers. The drugs' effect on PMN free oxygen radicals production may constitute an additional mechanism of their activity.
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