Skip to main content
SpringerLink
Log in

Cardiac Hypertrophy and Altered Cellular Electrical Activity of the Myocardium

Possible Electrophysiologic Basis for Myocardial Contractility Changes

  • Chapter
Physiology and Pathophysiology of the Heart

Part of the book series: Developments in Cardiovascular Medicine ((DICM,volume 34))

Abstract

The myocardial cell hypertrophies in response to a sustained increase in workload. Increased workload can result from factors including: pressure overload due to ventricular or systemic hypertension; volume overload because of an AV fistula, other defects in the heart pump, or hypervolemia; sustained increase in heart rate. It can be subsequent to regional damage brought about by acute or chronic ischemia and infarction, by nutritional and hormonal disturbances, and by dynamic [1] and isometric exercise [2]. There are numerous physiologic changes concomitant with and perhaps associated with hypertrophy of the myocardial cell. These include mechanical, biochemical, structural and ultrastructural, and most recently described, electrophysiologic alterations. The notion has developed that hypertrophy is compensatory, allowing the heart to meet the increased workload, and that cardiac failure ensues if hypertrophy is insufficient [3, 4]. The literature on hypertrophy and failure is extensive. This review will be limited to an examination of changes occurring in a common (and the most studied) form of hypertrophy, i.e., that provoked by pressure overload. We described the electrophysiologic changes associated with this form of hypertrophy and consider pertinent mechanical, structural, and biochemical data which are concomitant and may be related to the electrical changes. We will refer to other models or to naturally occurring disease-induced hypertrophy when they reflect areas of special significance or pertinence. The interested reader is directed to several recent reviews of biochemical changes in the myocardium during hypertrophy, including those of Rabinowitz and Zak [5], Wikman-Coffelt et al. [4], and Zak and Rabinowitz [6].

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Log in via an institution
Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 74.99
Price excludes VAT (USA)
  • Available as EPUB and PDF
  • Read on any device
  • Instant download
  • Own it forever

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Scheuer J, Tipton CM: Cardiovascular adaptation to physical training. Annu Rev Physiol 39: 221–251, 1977.

    Article  PubMed  CAS  Google Scholar 

  2. Muntz KH, Gonyea WJ, Mitchell JH: Cardiac hypertrophy in response to an isometric training program in the cat. Circ Res 49: 1092–1101, 1981.

    Article  PubMed  CAS  Google Scholar 

  3. Meerson FZ: The myocardium in hyperfunction, hypertrophy and heart failure. Circ Res (Suppl 2 ) 25: 1–163, 1969.

    Google Scholar 

  4. Wikman-Coffelt J, Parmley WW, Mason DJ: The cardiac hypertrophy process: analyses of factors determining pathological vs physiological development. Circ Res 45: 697–707, 1979.

    Article  PubMed  CAS  Google Scholar 

  5. Rabinowitz M, Zak R: Mitochondria and cardiac hypertrophy. Circ Res 36: 367–376, 1976.

    Article  Google Scholar 

  6. Zak R, Rabinowitz M: Molecular aspects of cardiac hypertrophy. Annu Rev Physiol 41: 539–552, 1969.

    Article  Google Scholar 

  7. Leyton RA, Sonnenblick EH: Ultrastructure of the failing heart. Am J Med Sci 258: 304–327, 1969.

    Article  PubMed  CAS  Google Scholar 

  8. Bishop SP, Cole CR: Ultrastructural changes in the canine myocardium with right ventricular hypertrophy and congestive heart failure. Lab Invest 20: 219–229, 1969.

    PubMed  CAS  Google Scholar 

  9. Lin HL, Katele KV, Grimm AF: Functional morphology of the pressure-and the volume-hypertrophied rat heart. Circ Res 41: 830–836, 1977.

    Article  PubMed  CAS  Google Scholar 

  10. Kawamura K, Konishi T: Symposium on function and structure of cardiac muscle. 1. Ultrastructure of the cell junction of heart muscle with special reference to its functional significance in excitation, conduction and to the concept of “disease of intercalated disc”. Jpn Circ J 31: 1533–1543, 1967.

    PubMed  CAS  Google Scholar 

  11. Sekiguchi M: Electron microscopical observation of the myocardium in patients with idiopathic cardiomyopathy using endomyocardial biopsy. J Mol Cell Cardiol 6: 111–122, 1974.

    Article  PubMed  CAS  Google Scholar 

  12. Kawamura K, James TN: Comparative ultrastructure of cellular junctions in working myocardium and the conduction system under normal and pathologic conditions. J Mol Cell Cardiol 3: 31–60, 1971.

    Article  PubMed  CAS  Google Scholar 

  13. Page E, McCallister LP: Quantitative electron microscopic description of heart muscle cells. Am J Cardiol 31: 172–181, 1973.

    Article  PubMed  CAS  Google Scholar 

  14. Meessen H: Ultrastructure of the myocardium: its significance in myocardial disease. Am J Cardiol 22: 319–327, 1968.

    Article  PubMed  CAS  Google Scholar 

  15. Wendt-Gallitelli MF, Jacob R: Time course of electron microscopic alterations in the hypertrophied myocardium of Goldblatt rats. Basic Res Cardiol 72: 209–213, 1977.

    Article  PubMed  CAS  Google Scholar 

  16. Goldstein MA, Sordahl LA, Schwartz A: Ultra-structural analysis of left ventricular hypertrophy in rabbits. J Mol Cell Cardiol 6: 265–273, 1974.

    Article  PubMed  CAS  Google Scholar 

  17. Aronson RS: Characteristics of action potentials of hypertrophied myocardium from rats with renal hypertension. Circ Res 47: 443–454, 1980.

    Article  PubMed  CAS  Google Scholar 

  18. Tomanek RJ, Banister EW: Myocardial ultrastructure after acute exercise stress with special reference to transverse tubules and intercalated discs. Cardiovasc Res 6: 671–679, 1972.

    Article  PubMed  CAS  Google Scholar 

  19. Horwood DM, Beznak M: Fluid and electrolyte shifts relating cardiac hypertrophy with normal growth. Can J Physiol Pharmacol 49: 951–958, 1971.

    Article  PubMed  CAS  Google Scholar 

  20. Anversa P, Loud AV, Giacomelli F, Wiener J: Absolute morphometric study of myocardial hypertrophy in experimental tension. Il. Ultrastructure of myocytes and interstitium. Lab Invest 38: 597–609, 1978.

    Article  PubMed  CAS  Google Scholar 

  21. Weiner J, Giacomelli F, Loud AV, Anversa P: Morphometry of cardiac hypertrophy induced by experimental renal hypertension. Am J Cardiol 44: 919–929, 1979.

    Article  Google Scholar 

  22. Breisch EA, Houser SR, Carey RA, Spann JF, Bove AA: Myocardial blood flow and capillary density in chronic pressure overload of the feline left ventricle. Cardiovasc Res 14: 469–475, 1980.

    Article  PubMed  CAS  Google Scholar 

  23. Cheitlin MD, Rabinowitz M, McAllister H, Hoffman JIE, Bharati S, Lev M: The distribution of fibrosis in the left ventricle in congenital aortic stenosis and coarctation of the aorta. Circulation 62: 823–830, 1980.

    Article  PubMed  CAS  Google Scholar 

  24. Gulch RW: The effect of chronic loading on the action potential of mammalian myocardium. J Mol Cell Cardiol 12: 415–420, 1980.

    Article  PubMed  CAS  Google Scholar 

  25. Rabinowitz M: Protein synthesis and turnover in normal and hypertrophied heart. Am J Cardiol 31: 202–210, 1973.

    Article  PubMed  CAS  Google Scholar 

  26. Schreiber SS, Rothschild MA, Oratz M: Investigation into the causes of increased protein synthesis in acute hemodynamic overload. In: Rona G, Ito Y (eds) Recent advances in studies on cardiac structure and metabolism, vol 12. Baltimore: University Park Press, 1978, pp 49–60.

    Google Scholar 

  27. Sims JM, Patzer B, Kumudavalli-Reddy M, Martin AF, Rabinowitz M, Zak R: The pathways of protein synthesis and degradation in normal heart and during development and regression of cardiac hypertrophy. In: Rona G, Ito Y (eds) Recent advances in studies on cardiac structure and metabolism, vol 12. Baltimore: University Park Press, 1978, pp 19–28.

    Google Scholar 

  28. Ueda S, Nagai R, Yayahi Y: Synthesis and enzymatic properties of myosin from hypertrophied and failing hearts: difference in behavior of right and left ventricular free walls and interventricular septum. In: Advances in: Tajuddin M, Das PK, Tarig M, Dhalla NS (eds) Advances in myocardiology, vol 1. Baltimore: University Park Press, 1980, pp 523–533.

    Google Scholar 

  29. Scheuer J, Bahn AK: Adenosine triphosphatase activity and physiological function. Circ Res 45: 112, 1979.

    Article  Google Scholar 

  30. Mercadier JJ, Lompre AM, Wisnewski C, Samuel JL, Bercovici J, Swynghedauw B, Schwartz K: Myosin isoenzymatic changes in several models of rat cardiac hypertrophy. Circ Res 49: 525–532, 1981.

    Article  PubMed  CAS  Google Scholar 

  31. Maughan D, Low E, Litten R III, Brayden J, Alpert N: Calcium activated muscle from hypertrophied rabbit hearts. Circ Res 44: 279–287, 1979.

    Article  PubMed  CAS  Google Scholar 

  32. Alpert NR, Mulieri LA: Increased myothermal economy of isometric force generation in compensated cardiac hypertrophy induced by pulmonary artery constriction in the rabbit: a characterization of heat liberation in normal and hypertrophied right ventricular papillary muscles. Circ Res 50: 49 1500, 1982.

    Google Scholar 

  33. Zimmer HG, Ibel H, Steinkopff G: Studies on the hexose monophosphate shunt in the myocardium during development of hypertrophy. In: Tajuddin M, Das PK, Tarig M, Dhalla NS (eds) Advances in myocardiology vol 1. Baltimore: University Park Press, 1980, pp 487–492.

    Google Scholar 

  34. Bonnin CM, Sparrow MP, Taylor RR: Collagen synthesis and content in right ventricular hypertrophy in the dog. Am J Physiol 241: h708 - h713, 1981.

    PubMed  CAS  Google Scholar 

  35. Frederiksen DW, Hoffnung JM, Frederiksen RT, Williams RB: The structural proteins of normal and diseased human myocardium. Circ Res 42: 459466, 1978.

    Google Scholar 

  36. Yabe Y, Abe H: Change in DNA synthesis in significantly hypertrophied human cardiac muscle. Tajddin M, Das PK, Tarig M, Dhalla MS (eds) Advances in myocardiology, vol 1. Baltimore: University Park Press, 1980, pp 553–564.

    Google Scholar 

  37. Hatt PY, Berjal G, Moraver J, Swynghedauw B: Heart failure: an electron microscopic study of the left ventrical papillary muscle in aortic insufficiency in the rabbit. J Mol Cell Cardiol 1: 235–247, 1970.

    Article  PubMed  CAS  Google Scholar 

  38. Hatt PY: Cellular changes and damage in mechanically overloaded hearts. In: Fleckenstein A, Rona G (eds) Recent advances in studies on cardiac structure and metabolism, vol 6. Baltimore: University Park Press, 1975, pp 325–334.

    Google Scholar 

  39. Spann JF, Buccino RA, Sonnenblick EH, Braunwald E: Contractile state of cardiac muscle obtained from cats with experimentally produced ventricular hypertrophy and heart failure. Circ Res 21: 34 1354, 1962.

    Google Scholar 

  40. Kaufman RL, Homburger H, Wirth H: Disorder in excitation-contraction coupling of cardiac muscle from cats with experimentally produced right ventricular hypertrophy. Circ Res 28: 346–357, 1971.

    Article  Google Scholar 

  41. Cooper G IV, Satavan M Jr, Harrison CE, Coleman HN III: Mechanisms for the abnormal energetics of the pressure induced hypertrophy of the cat myocardium. Circ Res 33: 213–223, 1973.

    Article  PubMed  Google Scholar 

  42. Meerson FZ, Kapelko VI: The contractile function of the myocardium in two types of cardiac adaptation to a chronic load. Cardiology 57: 183–199, 1972.

    Article  PubMed  CAS  Google Scholar 

  43. Williams JF Jr, Potter RD: Normal contractile state hypertrophied myocardium after pulmonary constriction in the cat. J Clin Invest 54: 1266 1272, 1974.

    Google Scholar 

  44. Cooper G IV, Tomanek RJ, Ehrhardt JC, Marcus ML: Chronic progressive pressure overload of the cat right ventricle. Circ Res 48: 488–497, 1981.

    Article  PubMed  Google Scholar 

  45. Natarajan G, Bove AA, Coulson RL, Carey RA, Spann JF: Increased passive stiffness of short term pressure overload hypertrophied myocardium in cat. Am J Physiol 237: H676 - H680, 1979.

    PubMed  CAS  Google Scholar 

  46. Williams JF Jr, Potter RD: Passive stiffness of pressure induced hypertrophied cat myocardium. Circ Res 49: 211–215, 1981.

    Article  PubMed  Google Scholar 

  47. Spann JF, Covell JW, Eckberg DL, Sonnenblick EH, Ross J, Braunwald E: Contractile performance of the hypertrophied and chronically failing cat ventricle. Am J Physiol 223: 1150–1157, 1972.

    PubMed  Google Scholar 

  48. Gelband H, Bassett AL: Depressed transmembrane potentials during experimentally induced ventricular failure in cats. Circ Res 32: 625–634, 1973.

    Article  PubMed  CAS  Google Scholar 

  49. Tritthart H, Leudcke H, Bayer R, Sterle H, Kauffmann R: Right ventricular hypertrophy in the cat: an electrophysiological and anatomical study. J Mol Cell Cardiol 7: 163–174, 1975.

    Article  PubMed  CAS  Google Scholar 

  50. Bassett AL, Gelband H: Chronic partial occlusion of the pulmonary artery in cats: change in ventricular action potential configuration during early hypertrophy. Circ Res 32: 15–26, 1973.

    Article  PubMed  CAS  Google Scholar 

  51. Bassett AL, Gelband H: Electrical and mechanical properties of cardiac muscle during chronic right ventricular pressure overload. In: Dhalla NS (ed) Myocardial biology. Recent advances in studies on cardiac structure and metabolism, vol 4. Baltimore: University Park Press, 1973, pp 3–20.

    Google Scholar 

  52. Ten Eick RE, Gelband H, Kahn J, Bassett AL: Changes in outward currents of papillary muscles of cats with right ventricle hypertrophy. Circulation 56:1I1–46, 1977.

    Google Scholar 

  53. Ten Eick RE, Bassett AL, Robertson LL: Severity of hypertrophy grades the changes induced in the myocardial action potential. Fed Proc, 1983 (1983).

    Google Scholar 

  54. Ten Eick RE, Bassett AL, Robertson LL: Possible electrophysiological basis for decreased contractility associated with myocardial hypertrophy in cat: a voltage clamp approach. In: Alpert N (ed) Perspectives in cardiovascular research, vol. 7: Myocardial hypertrophy and failure, New York, Raven Press, 1983, pp. 245–259.

    Google Scholar 

  55. Ten Eick RE, Gleband H, Goode M, Bassett AL: Increased inward rectifying potassium current in cat ventricle subjected to chronic pressure overload. Circulation 56: I1–77, 1978.

    Google Scholar 

  56. Bassett AL, Gelband H, Nilsson K, Myerburg RJ: Localized transmembrane action potential abnormalities in right ventricles subjected to pressure overload. Circulation 47: 11–47, 1977.

    Google Scholar 

  57. Aronson RS: Afterpotentials and triggered activity in hypertrophied myocardium from rats with renal hypertension. Circ Res 48: 720–727, 1981.

    Article  PubMed  CAS  Google Scholar 

  58. Alpert NR, Hamrell BB, Halpern W: Mechanical or biochemical correlates of cardiac hypertrophy. Circ Res (Suppl 2) 34 /35: 71–82, 1974.

    Google Scholar 

  59. Hamrell BB, Alpert NR: The mechanical characteristics of hypertrophied rabbit cardiac muscle in the absence of congestive heart failure: the contractile and series elastic elements. Circ Res 40: 20–25, 1977.

    Article  PubMed  CAS  Google Scholar 

  60. Konishi T: Electrophysiological study on the hypertrophied cardiac muscle experimentally produced in the rabbit. Jpn Circ J 29: 491–503, 1965.

    Article  PubMed  CAS  Google Scholar 

  61. Sharp NA: Alterations in ventricular action potentials in pressure overload and thyrotoxic hypertrophy. In: Alpert N (ed) Perspectives in cardiovascular research, vol. 7: Myocardial hypertrophy and failure, New York, Raven Press, 1983, pp. 245259.

    Google Scholar 

  62. Bassett AL, Myerburg RJ, Nilsson K, Sung RJ, Morales AR, Gelband H: Electrophysiologic consequences of experimental chronic left ventricular systolic hypertension. Circulation 4: 11–7, 1978.

    Google Scholar 

  63. Gulch RW, Baumann R, Jacob R: Analysis of myocardial action potential in left ventricular hypertrophy of the Goldblatt rats. Basic Res Cardiol 74: 6982, 1979.

    Google Scholar 

  64. Gulch RW: Alterations in excitation of mammalian myocardium as a function of chronic loading and their implications in the mechanical events. Basic Res Cardiol 75: 73–80, 1980.

    Article  PubMed  CAS  Google Scholar 

  65. Capasso JM, Strobeck JE, Sonnenblick EH: Myocardial mechanical alterations during gradual onset long term hypertension in rats. Am J Physiol 10: H435 - H441, 1981.

    Google Scholar 

  66. Jacob R, Ebrecht G, Kammereit A, Medugorac L, Wendt-Gallitelli MF: Myocardial function in different models of cardiac hypertrophy: an attempt at correlating mechanical, biochemical and morphological parameters. Basic Res Cardiol 72: 160–167, 1977.

    Article  PubMed  CAS  Google Scholar 

  67. Kammereit A, Jacob R: Alterations in rat myocardial mechanics under Goldblatt hypertension and experimental aortic stenosis. Basic Res Cardiol 74: 389–405, 1979.

    Article  PubMed  CAS  Google Scholar 

  68. Wendt-Gallitelli MF, Ebrecht G, Jacob R: Morphological alterations and their functional interpretation in the hypertrophied myocardium of Goldblatt hypertensive rats. J Mole Cell Cardiol 11: 275–287, 1979.

    Article  CAS  Google Scholar 

  69. Bing OHL, Matsushita S, Fanburg BL, Levine HJ: Mechanical properties of rat cardiac muscle during experimental hypertrophy. Circ Res 28: 234–245, 1971.

    Article  PubMed  CAS  Google Scholar 

  70. Jouannot P, Hatt PY: Rat myocardial mechanics during pressure induced hypertrophy development and reversal. Am J Physiol 299: 355–364, 1975.

    Google Scholar 

  71. Bing OHL, Fanburg BL, Brooks WW, Matsushita S: The effect of the lathyrogen R-aminoproprionitrile (BAPN) on the mechanical properties of experimentally hypertrophied rat cardiac muscle. Circ Res 43: 632–637, 1978.

    Article  PubMed  CAS  Google Scholar 

  72. Heller LJ: Augmented aftercontractions in papillary muscles from rats with cardiac hypertrophy. Am J Physiol 237: H649 - H654, 1979.

    PubMed  CAS  Google Scholar 

  73. Julian FJ, Morgan DL, Moss RL, Gonzalez M, Dwivedi P: Myocyte growth without physiological impairment in gradually induced rat cardiac hypertrophy. Circ Res 49: 1300–1310, 1981.

    Article  PubMed  CAS  Google Scholar 

  74. Tibbits GF, Barnard RJ, Baldwin DM, Cugalj N, Roberts NK: Influence of exercise on excitation contraction coupling in rat myocardium. Am J Physiol 240: H472 - H480, 1981.

    PubMed  CAS  Google Scholar 

  75. Jacob R, Brenner B, Ebrecht G, Holubarsch C, Medugorac I: Elastic contractile properties of the myocardium in experimental cardiac hypertrophy of the rat: methodological and pathophysiological considerations. Basic Res Cardiol 75: 253–261, 1980.

    Article  PubMed  CAS  Google Scholar 

  76. Holubarsch CH: Contractive type and fibrosis type of decreased myocardial distensibility: different changes in elasticity of myocardium in hypertension and hypertrophy. Basic Res Cardiol 75: 244–252, 1980.

    Article  PubMed  CAS  Google Scholar 

  77. Hayashi H, Shibata S: Electrical properties of cardiac cell membrane of spontaneously hypertensive rat. Eur J Pharmacol 27: 355–359, 1974.

    Article  CAS  Google Scholar 

  78. Heller LJ: Cardiac muscle mechanics from doca-and aging spontaneously hypertensive rats. Am J Physiol 235: H82 - H86, 1978.

    PubMed  CAS  Google Scholar 

  79. Heller LJ, Stauffer EK: Altered electrical and contractile properties of hypertrophied cardiac muscles. Fed Proc 38: 975, 1979.

    Google Scholar 

  80. Ferrier GR, Moe GK: Effect of calcium on acetylstrophanthidin-induced transient depolarizations in canine Purkinje tissue. Circ Res 33: 508–515, 1973.

    Article  PubMed  CAS  Google Scholar 

  81. Ferrier GR, Saunders JH, Mendez C: A cellular mechanism for the generation of ventricular arrhythmias by acetylstrophanthidin. Circ Res 32: 600–609, 1973.

    Article  PubMed  CAS  Google Scholar 

  82. Keung ECH, Aronson RS: Non-uniform electrophysiological properties and electrotonic interaction in hypertrophied rat myocardium. Circ Res 49: 150–158, 1981.

    Article  PubMed  CAS  Google Scholar 

  83. Keung ECH, Aronson RS: Transmembrane action potentials and the electrocardiogram in rats with renal hypertension. Cardiovasc Res 15: 611–614, 1981.

    Article  PubMed  CAS  Google Scholar 

  84. Coltart DJ, Meldrum SJ: Hypertrophic cardiomyopathy: an electrophysiological study. Br Med J 4: 217–218, 1970.

    Article  PubMed  CAS  Google Scholar 

  85. Singer DH, Baumgarten CM, Ten Eick RE: Cellular electrophysiology of ventricular and other dysrhythmias: studies on diseased and ischemic heart. Prog Cardiovasc Dis 24: 97–156, 1981.

    Article  PubMed  CAS  Google Scholar 

  86. Ten Eick RE, Baumgarten CM, Singer DH: Ventricular dysrhythmias: membrane basis, or, of currents, channels, gates and cables. Prog Cardiovasc Dis 24: 157–188, 1981.

    Article  PubMed  Google Scholar 

  87. Brorson L, Conradson TB, Olsson B, Varnauskas E: Right atrial monophasic action potential and effective refractory periods in relation to physical training and maximum heart rate. Cardiovasc Res 10: 160–168, 1976.

    Article  PubMed  CAS  Google Scholar 

  88. Bishop SP, Melsen LR: Myocardial necrosis, fibrosis and DNA synthesis in experimental cardiac hypertrophy induced by sudden pressure overload. Circ Res 39: 238–245, 1976.

    Article  PubMed  CAS  Google Scholar 

  89. Cutilletta AF, Benjamin M, Culpepper WS, Oparil S: Myocardial hypertrophy and ventricular performance in the absence of hypertension in spontaneously hypertensive rats. J Mol Cell Cardiol 10: 689–703, 1978.

    Article  PubMed  CAS  Google Scholar 

  90. Tomanek RJ, Davis JW, Anderson SC: The effects of alpha-methyldopa on cardiac hypertrophy in spontaneously hypertensive rats: ultrastructural, stereological and morphometric analysis. Cardiovasc Res 13: 173–182, 1979.

    Article  PubMed  CAS  Google Scholar 

  91. Dunn FG, Pfeffer MA, Frohlich ED: ECG alterations with progressive left ventricular hypertrophy in spontaneous hypertension. Clin Exp Hypertens 1: 67–86, 1978.

    Article  PubMed  CAS  Google Scholar 

  92. Mazzoleni A, Curtin ME, Wolfe R, Reiner L: On the relationship between heart weights, fibrosis, and QRS duration. J Electrocardiol 8: 233–236, 1975.

    Article  PubMed  CAS  Google Scholar 

  93. Kavaler F: Membrane depolarization as a cause of tension development in mammalian ventricular muscle. Am J Physiol 196: 968–970, 1959.

    Google Scholar 

  94. Morad M, Trautwein W: The effect of the duration of the action potential on contraction in the mammalian heart muscle. Pflugers Archiv 299: 66–82, 1968.

    Article  CAS  Google Scholar 

  95. Wood EH, Hoppner RL, Weidmann S: Inotropic effects of electrical currents. I. Positive and negative of constant electrical currents or current pulses applied during cardiac action potentials. II. Hypotheses: calcium movements, excitation contraction coupling and inotropic effects. Cir Res 24: 409–445, 1969.

    Article  CAS  Google Scholar 

  96. Beeler GW Jr, Reuter H: Relation between membrane potential, membrane current and activation of contraction in ventricular myocardial fibers. J Physiol 207: 211–229, 1970.

    PubMed  CAS  Google Scholar 

  97. Leoty C: Membrane currents and activation of contraction in rat ventricular fibers. J Physiol 239: 237–249, 1974.

    PubMed  CAS  Google Scholar 

  98. Lab MJ: Mechanically dependent changes in action potentials recorded from the intact frog ventricle. Circ Res 42: 519–528, 1978.

    Article  PubMed  CAS  Google Scholar 

  99. Spotnitz HM, Sonnenblick EH: Structural conditions in the hypertrophied and failing heart. Am J Cardiol 32: 398–406, 1973.

    Article  PubMed  CAS  Google Scholar 

  100. Morady F, Laks MM, Parmley WW: Comparison of sarcomere lengths from normal and hypertrophied inner and middle canine right ventricle. Am J Physiol 225: 1257–1259, 1973.

    PubMed  CAS  Google Scholar 

  101. Legato MJ: Cellular mechanisms of normal growth in the mammalian heart. II. A quantitative and qualitative comparison between the right and left ventricular myocytes in the dog from birth to five months of age. Circ Res 44: 263–279, 1979.

    Article  PubMed  CAS  Google Scholar 

  102. Bonnin CM, Sparrow MP, Taylor RR: Collagen synthesis and content in right ventricular hypertrophy in the dog. Am J Physiol 241: H708 - H713, 1981.

    PubMed  CAS  Google Scholar 

  103. Medugorac I: Characteristics of the hypertrophied left ventricular myocardium in Goldblatt rats. Basic Res Cardiol 72: 261–267, 1977.

    Article  PubMed  CAS  Google Scholar 

  104. Hemwall EL, Houser SR: Alterations of slow response action potentials in right ventricular hypertrophy. Circulation 66: 1I - 77, 1982.

    Article  Google Scholar 

  105. McDonald TF, Trautwein W: Membrane currents in cat myocardium: separation of inward and outward components. J Physiol 274: 193–216, 1978.

    PubMed  CAS  Google Scholar 

  106. Martin FG, Houser SR, Marino TA, Freeman AR: Comparison of normal and failing cardiac muscles: the drive related changes in extracellular potassium activity. Biophys J 37: 24, 1982.

    Google Scholar 

  107. Moulder PV, Eichelberger L, Daily PO: Segmental water and electrolyte distribution in canine hearts with right ventricular hypertrophy. Fed Proc 26: 382, 1967.

    Google Scholar 

  108. Nachev P: The effect of aortic coarctation on the concentration of water and electrolytes in cardiac muscle. Proc Soc Exp Biol Med 147: 137–139, 1974.

    PubMed  CAS  Google Scholar 

  109. Brutsaert DL, De Clerk NM, Gothals MA, Housmans PR: Relaxation of ventricular cardiac muscle. J Physiol 203: 469–480, 1978.

    Google Scholar 

  110. Le Carpentier Y, Martin JL, Gastineau P, Hatt PY: Load dependence of mammalian heart relaxation during cardiac hypertrophy and heart failure. Am J Physiol 242: H855 — H861, 1982.

    Google Scholar 

  111. Cooper G IV, Satava RM, Harrison CE, Coleman HN III: Normal myocardial function and energetics after reversing pressure overload hypertrophy. Am J Physiol 226: 1158–1165, 1974.

    PubMed  Google Scholar 

  112. Coulson RL, Yazdanfar S, Rubio E, Bove AA, Lemole GM, Spann JF: Recuperative potential of cardiac muscle following relief of pressure overload hypertrophy and right ventricular failure in the cat. Circ Res 40: 41–49, 1977.

    Article  PubMed  CAS  Google Scholar 

  113. Marcus ML, Eckberg DL, Braxmeier JL, Abboud FM: Effects of intermittent pressure loading on the development on ventricular hypertrophy in the cat. Circ Res 40: 484–488, 1977.

    Article  PubMed  CAS  Google Scholar 

  114. Capasso JM, Strobeck JE, Malhotra A, Scheuer J, Sonnenblick EH: Contractile behavior of rat myocardium after reversal of hypertensive hypertrophy. Am J Physiol 242: H882 — H889, 1982.

    PubMed  CAS  Google Scholar 

  115. Cutilletta AF, Dowell RT, Rudnik M, Arcilla RA, Zak R: Regression of myocardial hypertrophy. I. Experimental model, changes in heart weight, nucleic acids and collagens. J Mol Cell Cardiol 7: 767781, 1975.

    Google Scholar 

  116. Gibbons WR, Fozard HA: Voltage dependence and time dependence of contraction in sheep cardiac Purkinje fibers. Circ Res 28: 446–460, 1971.

    Article  PubMed  CAS  Google Scholar 

  117. Gibbons WR, Fozzard HA: Relationships between voltage and tension in sheep cardiac Purkinje fibers. J Gen Physiol 63: 345–366, 1975.

    Article  Google Scholar 

  118. Trautwein W, McDonald TF, Tripathi O: Calcium conductance and tension in mammalian ventricular muscle. Pflugers Archiv 354: 55–74, 1976.

    Google Scholar 

  119. Limas C, Limas CJ: Reduced number of (3-adrenergic receptors in the myocardium of spontaneously hypertensive rats. Biochem Biophys Res Commun 83: 710–714, 1978.

    Article  PubMed  CAS  Google Scholar 

  120. Woodcock EA, Funder JW, Johnston CI: Decreased cardiac (3-adrenergic receptors in deoxycorticosterone-salt and renal hypertensive rats. Circ Res 45: 560–565, 1979.

    Article  PubMed  CAS  Google Scholar 

  121. Cervoni P, Herzlinger H, Lai FM, Tanikella T: A comparison of cardiac reactivity and f3-adrenoceptor number and affinity between aorta-coarcted hypertensive and normotensive rats. Br J Pharmacol 74: 517–523, 1981.

    Article  PubMed  CAS  Google Scholar 

Download references

Authors
  1. Robert E. Ten Eick
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Arthur L. Bassett
    View author publications

    You can also search for this author in PubMed Google Scholar

Editor information

Editors and Affiliations

  1. Department of Physiology, University of Cincinnati Medical Center, 231 Bethesda Avenue, 45267, Cincinnati, Ohio, USA

    Nicholas Sperelakis

Rights and permissions

Reprints and permissions

Copyright information

© 1984 Springer Science+Business Media Dordrecht

About this chapter

Cite this chapter

Ten Eick, R.E., Bassett, A.L. (1984). Cardiac Hypertrophy and Altered Cellular Electrical Activity of the Myocardium. In: Sperelakis, N. (eds) Physiology and Pathophysiology of the Heart. Developments in Cardiovascular Medicine, vol 34. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-1171-4_25

Download citation

  • DOI: https://doi.org/10.1007/978-1-4757-1171-4_25

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4757-1173-8

  • Online ISBN: 978-1-4757-1171-4

  • eBook Packages: Springer Book Archive

Publish with us

Policies and ethics

Search

Navigation