Optical mapping of propagation changes induced by elevated extracellular potassium ion concentration in genetically altered mouse hearts. Punske, B., Rossi, S., Ershler, P., Rasmussen, I., & Abel, E. j-JE, 37 Suppl:128--134, 2004.
bibtex   
@Article{RSM:Pun2004,
  author =       "B.B. Punske and S. Rossi and P. Ershler and I.
                 Rasmussen and E.D. Abel",
  title =        "Optical mapping of propagation changes induced by
                 elevated extracellular potassium ion concentration in
                 genetically altered mouse hearts.",
  journal =      j-JE,
  year =         "2004",
  volume =       "37 Suppl",
  pages =        "128--134",
  robnote =      "Lack of insulin receptors in mouse myocytes has been
                 shown to reduce repolarizing potassium currents and
                 prolong action potential duration. We hypothesized that
                 these changes would manifest as rate-related effects on
                 electrical propagation in the intact heart. This study
                 employed optical mapping to characterize propagation
                 changes in intact mouse hearts with
                 cardiomyocyte-restricted knock out of insulin receptors
                 (CIRKO). None of the 8 CIRKO hearts maintained regular
                 responses to atrial stimulation at the 160 ms cycle
                 length under normal conditions; however, all of the WT
                 hearts were captured at this rate. Total activation
                 time for a 4 mm by 4 mm area was longer for CIRKO
                 hearts when compared with WT. Average epicardial
                 conduction velocity was slower for the CIRKO when
                 compared to WT. Propagation delay due to the presence
                 of high [K+]e was significant in both CIRKO and WT
                 mice, but significantly longer for the CIRKO hearts.
                 CONCLUSIONS: These results show that in addition to
                 reducing repolarization currents, impaired myocardial
                 insulin signaling leads to impaired electrical impulse
                 propagation particularly at increased heart rates.
                 These data suggest a link between impaired myocardial
                 insulin signaling and the increased risk of arrhythmia
                 and sudden death in patients with diabetes.",
  bibdate =      "Thu Dec 28 15:49:33 2006",
}

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