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Vitamin K Modulates Cardiac Action Potential by Blocking Sodium and Potassium Ion Channels

Institut de cardiologie de Québec, Hôpital Laval, Facultés de Pharmacie et de Médecine, Université Laval, Sainte-Foy, Québec, Canada, Centre de Recherche, Hôpital du Sacré-Cœur de Montréal

Annie Emond

B. Pharm

Institut de cardiologie de Québec, Hôpital Laval, Facultés de Pharmacie et de Médecine, Université Laval, Sainte-Foy, Québec, Canada

Vincent Fortin

Institut de cardiologie de Québec, Hôpital Laval

Pascal Daleau

Institut de cardiologie de Québec, Hôpital Laval

Guy Rousseau

Centre de Recherche, Hôpital du Sacré-Cœur de Montréal, Département de Pharmacologie, Faculté de Médecine

René Cardinal

Centre de Recherche, Hôpital du Sacré-Cœur de Montréal, Département de Pharmacologie, Faculté de Médecine

Jacques Turgeon

Institut de cardiologie de Québec, Hôpital Laval, Facultés de Pharmacie et de Médecine, Université Laval, Sainte-Foy, Québec, Canada, Centre de Recherche, Hôpital du Sacré-Cœur de Montréal, Département de Pharmacologie, Faculté de Médecine, Faculté de Pharmacie, Université de Montréal, Montréal, Québec, Canada

Background: Cardiovascular collapses, syncopes, and sudden deaths have been observed following the rapid administration of intravenous vitamin K. Our objectives were to characterize the effects of vitamin K on cardiac action potentials and to evaluate effects of vitamin K on sodium and potassium currents, namely I_Na, I _Kr, and I_Ks.

Methods and Results: Guinea pig hearts (n = 21) were paced at a cycle length of 250 msec and exposed to vitamin K at 1.15-4.6 µmol/L (2.5-10 mg/L). Monophasic action potential duration measured at 90% repolarization (MAPD₉₀) was not significantly reduced (-1.6 ± 0.3 msec; P > .05; N.S.) at 1.15 µmol/L, but increased by 6.5 ± 0.4 msec (P < .05) at 2.3 µmol/L. MAPD ₉₀ was not measurable at 4.6 µmol/L, as a result of inexcitability. Patch-clamp experiments in ventricular myocytes demonstrated a' ~50% reduction in I_Na by 10 µmol/L vitamin K and a concentration-dependent reduction of the K⁺ current elicited by short depolarizations (250 msec; I_K250). Estimated IC₅₀ for I_K250, mostly representing I_Kr, was 2.3 µmol/L. Vitamin K was less potent to block the K⁺ current elicited by long depolarizations (5,000 msec; IK₅₀₀₀), mostly representing I_Ks, with an estimated IC₅₀ over 100 µmol/L. Conclusions: Therapeutic concentrations (~1.5 µmol/L) of intravenous vitamin K modulate cardiac action potential by blocking ionic currents involved in cardiac depolarization and repolarization.

Key Words: potassium currents • sodium current • vitamin K • cardiac arrhythmia.

Journal of Cardiovascular Pharmacology and Therapeutics, Vol. 5, No. 4, 267-273 (2000)
DOI: 10.1054/JCPT.2000.16708


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