title: Vitamin K modulates cardiac action potential by blocking sodium and potassium ion channels.
abstract: 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).
  
  
  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 micromol/L (2.5-10 mg/L). Monophasic action potential duration measured at 90% repolarization (MAPD(90)) was not significantly reduced (-1.6 +/- 0.3 msec; P >.05; N.S.) at 1.15 micromol/L, but increased by 6.5 +/- 0.4 msec (P <.05) at 2.3 micromol/L. MAPD(90) was not measurable at 4.6 micromol/L, as a result of inexcitability. Patch-clamp experiments in ventricular myocytes demonstrated a approximately 50% reduction in I(Na) by 10 micromol/L vitamin K and a concentration-dependent reduction of the K(+) current elicited by short depolarizations (250 msec; I(K250)). Estimated IC(50) for I(K250), mostly representing I(Kr), was 2.3 micromol/L. Vitamin K was less potent to block the K(+) current elicited by long depolarizations (5,000 msec; I(K5000)), mostly representing I(Ks), with an estimated IC(50) over 100 micromol/L.
  
  
  CONCLUSIONS
  Therapeutic concentrations ( approximately 1.5 micromol/L) of intravenous vitamin K modulate cardiac action potential by blocking ionic currents involved in cardiac depolarization and repolarization.
authors.affiliation: Institut de cardiologie de Québec, Hôpital Laval et Université Laval, Sainte-Foy, Québec, Canada.
authors.forename: B
authors.initials: B
authors.lastname: Drolet
authors.forename: A
authors.initials: A
authors.lastname: Emond
authors.forename: V
authors.initials: V
authors.lastname: Fortin
authors.forename: P
authors.initials: P
authors.lastname: Daleau
authors.forename: G
authors.initials: G
authors.lastname: Rousseau
authors.forename: R
authors.initials: R
authors.lastname: Cardinal
authors.forename: J
authors.initials: J
authors.lastname: Turgeon
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D016757:Death, Sudden, Cardiac / Q000209:etiology; D004305:Dose-Response Relationship, Drug; D006168:Guinea Pigs; D006321:Heart / Q000187:drug effects / Q000502:physiology; D007262:Infusions, Intravenous; D015221:Potassium Channels / Q000187:drug effects* / Q000502:physiology; D015222:Sodium Channels / Q000187:drug effects* / Q000502:physiology; D013575:Syncope / Q000139:chemically induced / Q000503:physiopathology; D014812:Vitamin K / Q000008:administration & dosage / Q000494:pharmacology*
chemical_list: D015221:Potassium Channels; D015222:Sodium Channels; D014812:Vitamin K