Summary
Respiratory activity of the left ventricle of isolated perfused heart from rats with severe aortic constriction was examined by means of optical recording of intracellular redox changes. The speed of state-5-to-state-3 transition (recovery from short period of anoxia) was monitored fluorimetrically (PdN) and spectrophotometrically (cyt aa3).
Three days after stenosis of the abdominal aorta, the reoxidation of PdN was significantly accelerated, while the amplitude of the anoxic signal was rather comparable to that of control hearts. One week later, the rate of reduced NADH removal was considerably depressed.
Zusammenfassung
Die respiratorische Aktivität des linken Ventrikels beim isoliert-perfundierten Rattenherzen mit schwerer Aortenkonstriktion wurde durch optische Registrierung der intrazellulären Redoxänderungen untersucht. Die Geschwindigkeit des Übergangs vom Status 5 zum Status 3 (Erholung von kurzen Anoxieperioden) wurde fluorimetrisch (PdN) und spektrophotometrisch (cyt aa3) untersucht.
3 Tage nach Stenosierung der abdominalen Aorta war die Reoxidation der PdN signifikant beschleunigt, während die Amplitude des anoxischen Signals weitgehend der des Kontrollherzens vergleichbar waren. Eine Woche später war die Geschwindigkeit der NADH-Reoxidation beträchtlich vermindert.
Die Änderungen in der Fähigkeit der Mitochondrien, einen Überschuß an NADH zu oxidieren, scheint nicht mit einer veränderten Sauerstoffverfügbarkeit in Beziehung zu stehen, da sowohl die Geschwindigkeit der cyt-aa-3 Reoxidation und der Geschwindigkeit der Mb-Reoxigenation bei Vergleich der verschiedenen Gruppen bemerkenswert konstant war. Diese Änderungen reflektieren wahrscheinlich Veränderungen in der Organisation der respiratorischen Einheiten als solcher, oder sie sind Folge veränderter transmembranärer Translokationen, die bei der Kontrolle der Atmung beteiligt sind. Wie immer der wahre Mechanismus des beobachteten Phänomens beschaffen ist, so lassen die Ergebnisse auf jeden Fall eine Hemmung der Atmungskette am Ende der ersten Woche druckinduzierter Überbelastung vermuten.
Similar content being viewed by others
References
Albin, R., R. T. Dowell, H. Rabinowitz: Synthesis and degradation of mitochondrial component in hypertrophied rat heart. Bioch. J.131, 626 (1973).
Alpert, N.: Cardiac hypertrophy (London, New York, 1971).
Alpert, N. R., B. B. Harmell, W. Halpern: Mechanical and biochemical correlates of cardiac hypertrophy. Circul. Res.34–35 (suppl. II), 71 (1974).
Anversa, P., A. V. Loud, L. Vittali-Maza: Morphometry and autoradiography or early hypertrophic changes in the ventricular myocardium of the rat. Labor. Invest.35, 475 (1976).
Argus, M. F., J. C. Acros, V. M. Sardesai, J. L. Overby: Oxidative rates and phosphorylation in sarcosomes from experimentally induced failure of the rat heart. Proc. Soc. Exp. Biol. Med.117, 380 (1964).
Aschenbrenner, V., F. Druyan, R. Albin, M. Rabinowitz: Haem a cytochrome c and total protein turnover in mitochondria from rat heart and liver. Biochem. J.119, 157 (1970).
Bartosova, D., M. Chvapil, B. Horecky, O. Poupa, K. Rakusan, Z. Turek, M. Vizek: The growth of the muscular and collageneous parts of the heart in different types of cardiomegaly. J. Physiol. (London)200, 200 (1969).
Barlow, C.: Evaluation of cardiac ischemia by NADH fluorescence photography. Ann. Surg.186, 737 (1977).
Barlow, C., B. Chance: Ischemic areas in perfused rat hearts measurements by NADH fluorescence photograph. Science193, 909 (1976).
Chance, B., G. R. Williams: Respiratory enzymes in oxidative phosphorylation. III. The steady state. J. Biol. Chem.217, 409 (1955).
Chance, B., N. Graham: A rapid scanning dual wave-length spectrophotometer. Rev. Sci. Instr.42, 941 (1971).
Chance, B., M. Tamura, N. Oshino, T. Sackowitz: Criteria of cardiac anoxia and bioenergetic activity. Feder. Proc.33, 425A (1974).
Chance, B.: Pyridine nucleotide as an indicator of the oxygen requirements for energy-linked functions of mitochondria. Circul. Res.,38 (suppl. 1) 31 (1976).
Chapman, J. B.: Fluorimetric studies of oxidative metabolism in papillary muscle of the rabbit. J. Gen. Physiol.59, 135 (1972).
Chapman, J. B., C. L. Gibbs, D. S. Loiselle: Simultaneous heat and fluorescence changes in cardiac muscle at high rates of energy expenditure. J. Mol. Cell. Cardiol.9, 715 (1977).
Cooper, G., F. Puch, K. J. Zujko, C. E. Harrison, H. N. Coleman: Normal myocardial function and energetics in volume overloaded hypertrophy in cat. Circul. Res.32, 140 (1973).
Goldstein, M. A., L. Sordahl, A. Schwartz: Ultrastructural analysis of left ventricular hypertrophy in rabbits. J. Mol. Cell. Cardiol.6, 265 (1974).
Gross, N. J.: Control of mitochondrial turnover under the influence of thyroid hormone. J. Cell. Biol.48, 29 (1971).
Gunning, J. F., G. Cooper, G. E. Harrison, H. N. Coleman: Myocardial O2 consumption in experimental hypertrophy and congestive failure due to pressure overload. Amer. J. Cardiol.32, 427 (1973).
Gunning, J. F., N. H. Coleman: Myocardial oxygen consumption during experimental hypertrophy and congestive heart failure. J. Mol. Cell. Cardiol.5, 25 (1973).
Harigaya, S., A. Schwartz: Rate of calcium binding and uptake in normal animal and failing human cardiac muscle. Membrane vesicles and mitochondria. Circul. Res.25, 781 (1969).
Hatt, P. Y., G. Berjal, J. Moravec, B. Swynghedauw: Heart failure: an electron microscopic study of the left ventricular papillary muscle in aortic insufficience in the rabbit. J. Mol. Cell. Cardiol.I, 235 (1970).
Hatt, P. Y., P. Jouannot, J. Moravec, B. Swynghedauw: Current trends in heart hypertrophy. Basic. Res. Cardiol.69, 479 (1974).
Henquell, L.: Intercapillary distance and capillary reserve in hypertrophied rat heart beating in situ. Circul. Res.41, 400 (1977).
Jöbsis, F. F., J. C. Duffield: Oxidative and glycolytic recovery metabolism in muscle. Fluorometric observations in their relative contribution. J. Gen. Physiol.50, 1009 (1967).
Jöbsis, F. F., V. Legallais, M. O'Connor: A regulated differential fluorimeter for assay of oxidative metabolism in intact tissues. I. E. E. E. Trans. Bio. Med. Eng.13, 93 (1966).
Jouannot, P., P. Y. Hatt: Rat myocardial mechanics during pressure-induced hypertrophy and reversal. Amer. J. Physiol.229, 355 (1975).
Klingenberg, M.: The role of mitochondrial adenine nucleotide transport in the heart. In: Myocardial Failure,Richer, G., A. Weber, J. Goodwin 153–162 (Berlin 1977).
Korff von, R. W.: Metabolic characteristics of isolated rabbit heart mitochondria. J. Biol. Chem.240, 1351 (1965).
La Noue, K., J. Bryla, J. R. Williamson: Feed-back interactions in the control of citric acid cycle activity in rat heart mitochondria. J. Biol. Chem.247, 667 (1972).
Le Breton, A. C., P. C. Hoffmann: Ubiquinone and cytochrome b in isolated rat heart. J. Mol. Cell. Cardiol.9, 967 (1977).
Leger, J. J., K. Schwartz, B. Swynghedauw: Myosine et hypertrophie cardiaque. Pathol. Biol.25, 75 (1977).
Lehninger, A. L.: Ca++ transport by mitochondria and its possible role in cardiac relaxation cycle. Circul. Res.35 (suppl. III), 83 (1974).
Lindenmayer, G. E., L. A. Sordahl, A. Schwartz: Re-evaluation of oxidative phosphorylation in cardiac mitochondria from animals with heart failure. Circul. Res.23, 439 (1968).
Lübbers, D. W., W. Niessel: Rapid spectrophotometer for rabbit heart perfused with hemoglobine-free solution. Pflüg. Arch. Physiol.268, 286 (1959).
Martin, A. F., M. K. Reddy, R. Zak, R. T. Dowell, M. Rabinowitz: Protein metabolism in hypertrophied heart muscle. Circul. Res.35 (suppl. III) 32 (1974).
Meerson, F. Z.: The myocardium in hyperfunction hypertrophy and heart failure. Circul. Res.25 (suppl. II) 163 (1969).
Meerson, F. Z.: Insufficiency of hypertrophied heart. Basic Res. Cardiol.71, 343 (1976).
Mochet-Moravec, M., V. Aschenbrenner: Morphological and biochemical correlates of mitochondrial metabolism in hypertrophied and failing heart. Physiol. Bohemoslov.25, 459A (1976).
Moravec, J.: Contribution à l'étude des mitochondries cardiaques. Thèse d'Etat ès Sciences, Université Paris-Sud, Orsay, Juillet (1975).
Moravec, J., A. Corsin, P. Y. Hatt: Dependence of myocardial redox systems on the concentration of exogenous substrate. In: Recent Advances in Studies on Cardiac Structure and Metabolism, vol. 10,Roy, P. E., P. Harris (eds) 167–177 (Baltimore 1975).
Moravec, J., A. Corsin, P. Owen, L. H. Opie: Effect of increased aortic perfusion pressure on the fluorescence emission of isolated rat heart. J. Mol. Cell. Cardiol.6, 187 (1974).
Olson, R. E., D. A. Piatnek: Conservation of energy in cardiac muscle. Ann. N. Y. Acad. Sci.72, 466 (1959).
Opie, L. H.: Metabolism of the heart in health and disease. Amer. H. J.77, 100 (1969).
Pool, P. E., J. F. Spann, R. A. Buccino, E. H. Sonnenblick, E. Braunwald: Myocardial high energy phosphate stores in cardiac hypertrophy and heart failure. Circul. Res.21, 365 (1967).
Pool, P. E.: Energy stores and energy utilization in the myocardium in hypertrophy and heart failure. In: Cardiac Hypertrophy,Albert, N. 539–549 (N. Y., London 1971).
Rabinowitz, M., V. Aschenbrenner, R. Albin, N. J. Gross, R. Zak, K. G. Nair: Synthesis and turnover of heart mitochondria in normal hypertrophied and hypoxic rat. In: Cardiac Hypertrophy,Alpert, N. 283–300 (N. Y., London 1971).
Rabinowitz, M., R. Zak: Biochemical and cellular changes in cardiac hypertrophy. Ann. Rev. Med.23, 245 (1972).
Raczniak, T. J., C. F. Chesney, J. R. Allen: Oxidative phosphorylation and respiration by mitochondria from normal hypertrophied and failing rat hearts. J. Mol. Cell. Cardiol.9, 215 (1977).
Schwartz, A., K. P. Lee: Study of heart mitochondria and glycolytic metabolism in experimentally induced cardiac failure. Circul. Res.10, 321 (1962).
Schwartz, A.: Studies on mitochondria from normal hypertrophied and failing myocardium. In: Cardiac Hypertrophy,Alpert, N., 511–538 (N. Y., London, 1971).
Schwartz, A., L. A. Sordahl, M. L. Entman, J. C. Allen, Y. S. Reddy, M. Goldstein, R. J. Luchi, L. E. Wyborny: Abnormal biochemistry in myocardial failure. Amer. J. Cardiol.32, 407 (1973).
Seiden, D.: A quantitative analysis of muscle cell changes in compensatory hypertrophy and work-induced hypertrophy. Amer. J. Anat.145, 459 (1976).
Shiverick, K. T., B. B. Hamrell, N. R. Alpert: Structural and functional properties of myosine associated with the compensatory cardiac hypertrophy in the rabbit. J. Mol. Cell. Cardiol.8, 837 (1976).
Sobel, B. E., J. F. Spann, P. E. Pool, E. H. Sonnenblick, E. Braunwald: Normal oxidative phosphorylation in mitochondria from failing heart. Circul. Res.21, 355 (1967).
Sordahl, L. A., W. B. Mc Collum, W. G. Wood: Motochondria and s. r. function in cardiac hypertrophy and failure. Amer. J. Physiol.224, 497 (1973).
Swynghedauw, B., F. Wanstok, D. Courtault: Les effets du 2,4 dinitrophenol sur l'hypertrophie cardiaque expérimentale chez le rat. Pathol. Biol.16, 667 (1968).
Swynghedauw, B.: The myosine isozyme hypothesis in chronic heart overloading. J. Mol. Cell. Cardiol.8, 915 (1976).
Tamura, M., N. Oshino, B. Chance: A new spectroscopic approach into cardiac energy metabolism. 8th Internat. Meeting of ISGRCM, Tokyo, May 26–29 (1976).
Wendt, I. R., J. B. Chapman: Fluorimetric studies of recovery metabolism of rat fast and slow-twich muscles. Amer. J. Physiol.230, 1644 (1976).
Williams, J. N.: A method for simultaneous quantitative estimation of cytochrome a, b, c1 and c in mitochondria. Arch. Biochem. Biophys.107, 537 (1964).
Wollenberger, A., W. Schultze: Mitochondrial alterations in the myocardium of dogs with aortic stenosis. J. Biophys. Biochem. Cytol.10, 285 (1961).
Wollenberger, A., B. Kleitke, W. Schultze: The conditioning of the mitochondria in the hypertrophied hearts of dogs with slowly developing stenosis of the aorta. Acta Biol. Med. German17, 334 (1966).
Author information
Authors and Affiliations
Additional information
With 5 figures and 2 tables
Rights and permissions
About this article
Cite this article
Moravec, J., Renault, G. & Hatt, P.Y. Alterations of mitochondrial function as detected in left ventricular myocardium of rats with acute aortic constriction. Basic Res Cardiol 73, 535–550 (1978). https://doi.org/10.1007/BF01906792
Received:
Issue Date:
DOI: https://doi.org/10.1007/BF01906792