Journal of Molecular and Cellular Cardiology
Volume 42, Issue 2 , Pages 315-325 , February 2007

Ionic basis of ischemia-induced bradycardia in the rabbit sinoatrial node

  • Yi-Mei Du

      Affiliations

    • Department of Physiology, Texas Tech University Health Sciences Center, 3601 Fourth Street, Lubbock, TX 79430, USA
    • Department of Physiology, Tongji Medical College of Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan 430030, China
    • ,
  • Richard D. Nathan

      Affiliations

    • Department of Physiology, Texas Tech University Health Sciences Center, 3601 Fourth Street, Lubbock, TX 79430, USA
    • Corresponding Author InformationCorresponding author. Tel.: +806 743 2536; fax: +806 743 1512.

Received 11 May 2006 ,Revised 3 October 2006 ,Accepted 4 October 2006.

References 

  1. Ornato JP, Peberdy MA. The mystery of bradyasystole during cardiac arrest. Ann. Emerg. Med. 1996;27:576–587
  2. Gaul GB, Gruska M, Titscher G, Blazek G, Havelec L, Marktl W, et al. Prediction of survival after out-of-hospital cardiac arrest: results of a community-based study in Vienna. Resuscitation. 1996;32:169–176
  3. Moffat MP. Concentration-dependent effects of prostacyclin on the response of the isolated guinea pig heart to ischemia and reperfusion: possible involvement of the slow inward current. J. Pharmacol. Exp. Ther. 1987;242:292–299
  4. Chiba S, Simmons TW, Levy MN. Chronotropic responses to experimental ischemia of the canine sino auricular node. Arch. Int. Physiol. Biochim. 1976;84:81–88
  5. Motomura S, Hashimoto K. Reperfusion-induced bradycardia in the isolated, blood perfused sino-atrial node and papillary muscle preparations of the dog. Jpn. Heart J. 1982;23(Suppl.):112–115
  6. Senges J, Mizutani T, Pelzer D, Brachmann J, Sonnhof U, Kübler W. Effect of hypoxia on the sinoatrial node, atrium, and atrioventricular node in the rabbit heart. Circ. Res. 1979;44:856–863
  7. Nishi K, Yoshikawa Y, Sugahara K, Morioka T. Changes in electrical activity and ultrastructure of sinoatrial nodal cells of the rabbit's heart exposed to hypoxic solution. Circ. Res. 1980;46:201–213
  8. Kohlhardt M, Mnich Z, Maier G. Alterations of the excitation process of the sinoatrial pacemaker cell in the presence of anoxia and metabolic inhibitors. J. Mol. Cell. Cardiol. 1977;9:477–488
  9. Yoshikawa Y, Kano T, Higuchi M, Nishi K. Effects of coenzyme Q10 on recovery of hypoxia-induced changes in ATP and creatine phosphate contents of sinoatrial nodal cells of the rabbit's heart after reoxygenation. Arch. Int. Pharmacodyn. Ther. 1987;287:96–108
  10. Carmeliet E. Cardiac ionic currents and acute ischemia: from channels to arrhythmias. Physiol. Rev. 1999;79:917–1017
  11. Han X, Habuchi Y, Giles WR. Effects of metabolic inhibition on action potentials and ionic currents in cardiac pacemaking cells. Circulation. 1994;90(Suppl. I):582;(Abstract)
  12. Han X, Light PE, Giles WR, French RJ. Identification and properties of an ATP-sensitive K+ current in rabbit sino-atrial node pacemaker cells. J. Physiol. 1996;490:337–350
  13. Gryshchenko O, Qu J, Nathan RD. Ischemia alters the electrical activity of pacemaker cells isolated from the rabbit sinoatrial node. Am. J. Physiol. 2002;282:H2284–H2295
  14. Boyett MR, Honjo H, Kodama I. The sinoatrial node, a heterogeneous pacemaker structure. Cardiovasc. Res. 2000;47:658–687
  15. Verheijck EE, Wessels A, van Ginneken ACG, Bourier J, Markman MWM, Vermeulen JLM, et al. Distribution of atrial and nodal cells within the rabbit sinoatrial node: models of sinoatrial transition. Circulation. 1998;97:1623–1631
  16. Fan JS, Palade P. Perforated patch recording with beta-escin. Pflugers Arch. 1998;436:1021–1023
  17. Bean BP. Nitrendipine block of cardiac calcium channels: high-affinity binding to the inactivated state. Proc. Natl. Acad. Sci. 1984;81:6388–6392
  18. Cohen CJ, Spires S, Van Skiver D. Block of T-type Ca channels in guinea pig atrial cells by antiarrhythmic agents and Ca channel antagonists. J. Gen. Physiol. 1992;100:703–728
  19. Li J, Qu J, Nathan RD. Ionic basis of ryanodine's negative chronotropic effect on pacemaker cells isolated from the sinoatrial node. Am. J. Physiol. 1997;273:H2481–H2489
  20. Barry PH, Lynch JW. Liquid junction potentials and small cell effects in patch-clamp analysis. J. Membr. Biol. 1991;121:101–117
  21. Isenberg G, Klockner U. Calcium tolerant ventricular myocytes prepared by preincubation in a “KB medium”. Pflugers Arch. 1982;395:6–18
  22. Kléber AG, Riegger CB, Janse MJ. Extracellular K+ and H+ shifts in early ischemia: mechanisms and relation to changes in impulse propagation. J. Mol. Cell. Cardiol. 1987;19(Suppl. 5):35–44
  23. Mohabir R, Lee H-C, Kurz RW, Clusin WT. Effects of ischemia and hypercarbic acidosis on myocyte calcium transients, contraction, and pHi in perfused rabbit hearts. Circ. Res. 1991;69:1525–1537
  24. Kimura S, Bassett AL, Furukawa T, Cuevas J, Myerburg RJ. Electrophysiological properties and responses to simulated ischemia in cat ventricular myocytes of endocardial and epicardial origin. Circ. Res. 1990;66:469–477
  25. Kimura J, Miyamae S, Noma A. Identification of sodium–calcium exchange current in single ventricular cells of guinea-pig. J. Physiol. 1987;384:199–222
  26. Beuckelmann DJ, Wier WG. Sodium–calcium exchange in guinea-pig cardiac cells: exchange current and changes in intracellular Ca2+. J. Physiol. 1989;414:499–520
  27. Zhou Z, Lipsius SL. Na+–Ca2+ exchange current in latent pacemaker cells isolated from cat right atrium. J. Physiol. 1993;466:263–285
  28. Ju Y-K, Allen DG. Intracellular calcium and Na+–Ca2+ exchange current in isolated toad pacemaker cells. J. Physiol. 1998;508:153–166
  29. Hüser J, Blatter LA, Lipsius SL. Intracellular Ca2+ release contributes to automaticity in cat atrial pacemaker cells. J. Physiol. 2000;524:415–422
  30. Bogdanov KY, Vinogradova TM, Lakatta EG. Sinoatrial node cell ryanodine receptor and Na+–Ca2+ exchanger: molecular partners in pacemaker regulation. Circ. Res. 2001;88:1254–1258
  31. Sanguinetti MC, Jurkiewicz NK. Two components of cardiac delayed rectifier K+ current: differential sensitivity to block by class III antiarrhythmic agents. J. Gen. Physiol. 1990;96:195–215
  32. Busch AE, Suessbrich H, Waldegger S, Sailer E, Greger R, Lang H-J, et al. Inhibition of IKs in guinea pig cardiac myocytes and guinea pig IsK channels by the chromanol 293B. Pflugers Arch. 1996;432:1094–1096
  33. Ju Y-K, Allen DG. Early effects of metabolic inhibition on intracellular Ca2+ in toad pacemaker cells: involvement of Ca2+ stores. Am. J. Physiol. 2003;284:H1087–H1094
  34. Ellingsen O, Davidoff AJ, Prasad SK, Berger HJ, Springhorn JP, Marsh JD, et al. Adult rat ventricular myocytes cultured in defined medium: phenotype and electromechanical function. Am. J. Physiol. 1993;265:H747–H754
  35. Hagiwara N, Irisawa H, Kameyama M. Contribution of two types of calcium currents to the pacemaker potentials of rabbit sino-atrial node cells. J. Physiol. 1988;395:233–253
  36. Doerr T, Denger R, Trautwein W. Calcium currents in single SA nodal cells of the rabbit heart studied with action potential clamp. Pflugers Arch. 1989;413:599–603
  37. Krafte DS, Kass RS. Hydrogen ion modulation of Ca channel current in cardiac ventricular cells: evidence for multiple mechanisms. J. Gen. Physiol. 1988;91:641–657
  38. Komukai K, Pascarel C, Orchard CH. Compensatory role of CaMKII on ICa and SR function during acidosis in rat ventricular myocytes. Pflugers Arch. 2001;442:353–361
  39. Vinogradova TM, Zhou Y-Y, Bogdanov KY, Yang D, Kuschel M, Cheng H, et al. Sinoatrial node pacemaker activity requires Ca2+/calmodulin-dependent protein kinase II activation. Circ. Res. 2000;87:760–767
  40. Mubagwa K. Sarcoplasmic reticulum function during myocardial ischaemia and reperfusion. Cardiovasc. Res. 1995;30:166–175
  41. Habuchi Y, Noda T, Nishimura M, Watanabe Y. Recovery of the slow inward current from Ca2+-mediated and voltage-dependent inactivation in the rabbit sinoatrial node. J. Mol. Cell. Cardiol. 1990;22:469–482
  42. Tseng G-N, Boyden PA. Different effects of intracellular Ca and protein kinase C on cardiac T and L Ca currents. Am. J. Physiol. 1991;261:H364–H379
  43. Tytgat J, Nilius B, Carmeliet E. Modulation of the T-type cardiac Ca channel by changes in proton concentration. J. Gen. Physiol. 1990;96:973–990
  44. Earm YE, Irisawa H. Effects of pH on the Na–Ca exchange current in single ventricular cells of the guinea pig. Jpn. Heart J. 1986;27(Suppl. 1):153–158
  45. Doering AE, Lederer WJ. The mechanism by which cytoplasmic protons inhibit the sodium–calcium exchanger in guinea-pig heart cells. J. Physiol. 1993;466:481–499
  46. Egger M, Niggli E. Paradoxical block of the Na+–Ca2+ exchanger by extracellular protons in guinea-pig ventricular myocytes. J. Physiol. 2000;523:353–366
  47. Shibasaki T. Conductance and kinetics of delayed rectifier potassium channels in nodal cells of the rabbit heart. J. Physiol. 1987;387:227–250

PII: S0022-2828(06)00960-6

doi: 10.1016/j.yjmcc.2006.10.004

Journal of Molecular and Cellular Cardiology
Volume 42, Issue 2 , Pages 315-325 , February 2007

Article Tools

* Image Usage & Resolution