• DocumentCode
    2819636
  • Title

    Effect of Na+-K+ pump inhibition on extracellular potassium accumulation during myocardial ischemia: a simulation study

  • Author

    Rodríguez, B. ; Ferrero, JM, Jr.

  • Author_Institution
    DIE, Univ. Politecnica de Valencia, Spain
  • fYear
    2000
  • fDate
    2000
  • Firstpage
    315
  • Lastpage
    318
  • Abstract
    Acute myocardial ischemia leads to fast extracellular K+ accumulation and subsequent development of reentrant arrhythmias. Despite the importance of this phenomenon, mechanisms responsible for cellular K+ loss are still unknown. One possible cause is a decrease of K+ influx due to a partial inhibition of Na+-K+ pump activity. The maximum Na +-K+ pump current of Luo-Rudy phase II action potential model was modified to study the effect of pump inhibition on extracellular potassium accumulation in the absence of coronary flow. The authors´ results show that Na+-K+ pump inhibition could considerably contribute to extracellular K+ accumulation during acute myocardial ischemia. However, since a decrease of INaKNAK reduces KC driving force and K+ outward current, other mechanisms than Na+-K+ pump inhibition should necessarily contribute to the enhancement of unidirectional K+ efflux experimentally observed during acute myocardial ischemia
  • Keywords
    bioelectric phenomena; biomembrane transport; cardiology; muscle; physiological models; potassium; sodium; K; K+ outward current; Luo-Rudy phase II action potential model; Na; Na+-K+ pump inhibition effect; acute myocardial ischemia; cardiac electrophysiology; coronary flow; extracellular potassium accumulation; myocardial ischemia; partial inhibition; unidirectional K+ efflux; Cardiology; Computational modeling; Computer simulation; Equations; Extracellular; Ischemic pain; Microcomputers; Monitoring; Myocardium; Zinc;
  • fLanguage
    English
  • Publisher
    ieee
  • Conference_Titel
    Computers in Cardiology 2000
  • Conference_Location
    Cambridge, MA
  • ISSN
    0276-6547
  • Print_ISBN
    0-7803-6557-7
  • Type

    conf

  • DOI
    10.1109/CIC.2000.898520
  • Filename
    898520