Abstract
Atrophy of the rat heart induced by hemodynamic unloading after heterotopic transplantation is associated with impaired relaxation while systolic function remains normal when compared to the heart of the recipient animal. To identify possible underlying mechanisms for the above, we studied some aspects of membrane calcium handling using postextrasystolic potentiation of contractions in the isolated right ventricular papillary muscle and in the left ventricle of the Langendorff-perfused heart. We also compared the alterations of the unloaded heart with those of overloaded hypertrophic hearts of rats with suprarenal aortic constriction. In the atrophic heart the degree of potentiation after one extrasystole, considered to be proportional to the trans-sarcolemmal influx of Ca2+ during an action potential, was increased by 125% when compared with recipient hearts. The rate of decay of potentiation which reflects the fraction of activator Ca2+ recirculating in the cells via the sarcoplasmic reticulum, negatively correlated with the degree of potentiation, although its mean value was not significantly altered. In hypertrophic hearts the decay of potentiation was faster when compared with the hearts of sham-operated animals, indicating a decreased recirculating fraction of Ca2+. The data suggest that the relative importance of trans-sarcolemmal Ca2+ fluxes is increased both in cardiac atrophy and hypertrophy, but their quantitative role in the control of cardiac contraction might differ.
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References
Campbell SE, Korecky B, Rakusan K (1991) Remodeling of myocyte dimensions in hypertrophic and atrophic rat hearts. Circ Res 68: 984–996
Campbell SE, Rakusan K, Gerdes AM (1989) Change in cardiac myocyte size distribution in aortic-constricted neonatal rats. Basic Res Cardiol 84: 247–258
Curtis MJ, MacLeod BA, Tabrizchi R, Walker MJA (1985) An improved perfusion apparatus for small animal hearts. J Pharmacol Meth 15: 87–94
Ezzaher A, Bouanani NEH, Su JB, Hittinger L, Crozatier B (1994) Increased negative inotropic effect of calciumchannel blockers in hypertrophied and failing rabbit heart. J Pharmacol Exp Ther 257: 466–471
Gilligan JP, Spector S (1984) Synthesis of collagen in cardiac and vascular walls. Hypertension 6 (suppl III): 44–49
Gwathmey JK, Morgan JP (1985) Altered calcium handling in experimental pressure-overload hypertrophy in the ferret. Cir Res 57: 836–843
Klein I, Hong C, Schreiber SS (1990) Cardiac atrophy in the heterotopically transplanted rat heart: in vitro protein synthesis. J Mol Cell Cardiol 22: 461–468
Kolář F, MacNaughton C, Papouŝek F, Korecky B (1993) Systolic mechanical performance of heterotopically transplanted hearts in rats treated with cyclosporin. Cardiovasc Res 27: 1244–1247
Komuro I, Kurabayashi M, Shibazaki Y, Takaku F, Yazaki Y (1989) Molecular cloning and characterization of a Ca2++Mg2+-dependent adenosine triphosphatase from rat cardiac sarcoplasmic reticulum. Regulation of its expression by pressure overload and developmental stage. J Clin Invest 83: 1102–1108
Korecky B, Ganguly PK, Elimban V, Dhalla NS (1986) Muscle mechanics and Ca2+ transport in atrophic heart transplants in rat. Amer J Physiol 251: H941-H950
Korecky B, Rakusan K (1983) Morphological and physiological aspects of cardiac atrophy. In: Alpert NR (ed) Perspectives in Cardiovascular Research (vol 7): Myocardial Hypertrophy and Failure; Raven Press, New York, pp 293–309
Korecky B, Zak R, Schwartz K, Aschenbrenner V (1987) Role of thyroid hormone in regulating isomyosin composition, contractility and size of heterotopically isotransplanted rat heart. Circ Res 60: 824–830
Lamers JMJ, Stinis JT (1979) Defective calcium pump in the sarcoplasmic reticulum of the hypertrophied rabbit heart. Life Sci 24: 2313–2320
Lee S, Willoughby WF, Smallwood CJ, Dawson A, Orlow MJ (1970) Heterotopic heart and lung transplantation in the rat. Am J Pathol 59: 279–298
Levitsky D, de la Bastie D, Schwartz K, Lompré A-M (1991) Ca2+-ATPase and function of sarcoplasmic reticulum during cardiac hypertrophy. Am J Physiol 261 (suppl): 23–26
Rohlíĉek V (1973) A photoelectric forcetransducer. Physiol Bohemoslov 22: 89
Rohlíĉek V (1989) A microcomputerbased analyser for evaluation of contractile properties of a cardiac muscle. Physiol Res 38: 389–401
Shekonin B, Korecky B (1992) Alterations of extracellular matrix in cardiac atrophy. In: Oštádal B, Dhalla NS (eds) Heart Function in Health and Diseaser Kluwer Acad Publ, Boston, pp 321–335
Schouten VJA, Bucx JJJ, de Tombe PP ter Keurs HEDJ (1990) Sarcolemma, sarcoplasmic reticulum, and sarcomeres as limiting factors in force production in rat heart. Circ Res 67: 913–922
Schouten VJA, van Deen JK, de Tombe P, Verveen AA (1987) Force-interval relationship in heart muscle of mammals: A calcium compartment model. Biophys J 51: 13–26
Schouten VJA, Vliegen HW, van der Laarse A, Huysmans HA (1990) Altered calcium handling at normal contractility in hypertrophied rat heart. J Mol Cell Cardiol 22: 987–998
Schwartz K, Carrier L, Lompré A-M, Mercadier J-J, Boheler KR (1992) Contractile proteins and sarcoplasmic reticulum calcium-ATPase gene expression in the hypertrophied and failing heart. In: Hasenfuss G, Holubarsch C, Just H, Alpert NR (eds) Cellular and Molecular Alterations in the Failing Human Heart; Steinkopff Verlag, Darmstadt, pp 285–290
Wohlfart B, Noble MIM (1982) The cardiac excitation-contraction cycle. Pharmacol Ther 16: 1–43
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Kolář, F., MacNaughton, C., Papoušek, F. et al. Changes in calcium handling in atrophic heterotopically isotransplanted rat hearts. Basic Res Cardiol 90, 475–481 (1995). https://doi.org/10.1007/BF00788540
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DOI: https://doi.org/10.1007/BF00788540