Quinidine attenuates sympathetically induced poststenotic myocardial ischemia.
Beside its antiarrhythmic properties, which in particular are used for the treatment of atrial fibrillation, quinidine is known to have alpha-adrenoceptor blocking properties. On the other hand, atrial fibrillation is reported to cause activation of the sympathetic nervous system which, in turn, reduces coronary blood flow when the coronary reserve is already compromised. Therefore, we tested the effect of quinidine (3 mg/kg i.v.) on the coronary vasculature during electrical stimulation of cardiac sympathetic nerves in the presence and absence of a stenosis on the left circumflex coronary artery. In 7 anesthetized dogs the end-diastolic distal coronary resistance during cardiac sympathetic nerve stimulation in the presence of a severe stenosis on the left circumflex coronary artery increased by 18% before, and decreased by 17% after administration of quinidine. We conclude that quinidine inhibits the vasoconstriction of poststenotic coronary arteries during cardiac sympathetic nerve stimulation and thus might prevent a poststenotic stress-induced myocardial ischemia.
D000317:Adrenergic alpha-Antagonists; D000818:Animals; D003251:Constriction, Pathologic; D003326:Coronary Circulation / Q000187:drug effects; D003327:Coronary Disease / Q000503:physiopathology* / Q000517:prevention & control; D004285:Dogs; D004558:Electric Stimulation; D006321:Heart / Q000294:innervation*; D011802:Quinidine / Q000494:pharmacology*; D013564:Sympathetic Nervous System / Q000187:drug effects*
D000317:Adrenergic alpha-Antagonists; D011802:Quinidine