Effect of aortic constriction on rat heart function and mortality

  • H.-G. Zimmer
Conference paper


The maximal rate of rise of left ventricular pressure (LV dP/dtmax) measured in closed-chest rats by means of an ultraminiature catheter pressure transducer served as an indicator of cardiac contractility (6). It was slightly increased subsequent to constriction of the abdominal aorta and markedly enhanced after administration of isoproterenol and triiodothyronine. In all three models of cardiac hypertrophy, the enhancement of contractility occurred prior to the maximal stimulation of myocardial adenine nucleotide and protein synthesis. Combination of severe aortic constriction with simultaneous administration of isoproterenol induced an impairment of rat heart function. 24 hours after this intervention, heart rate, left ventricular systolic pressure, and LV dP/dtmax were all depressed by more than 20 %, and the content of cardiac ATP was also diminished to about the same extent. The mortality of rats with severe aortic constriction, which was 46 % when physiologic saline was applied as continuous i.v. infusion for 48 hours, was reduced to 18 % by ribose.

Key words

adenine nucleotide biosynthesis afterload cardiac ATP content cardiac contractility cardioprotection isoproterenol triiodothyronine 


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  1. 1.
    Bergey, J. L., K. Nocella, J. D. McCallum: Acute coronary artery occlusion-reperfusion-induced arrhythmias in rats, dogs and pigs: Antiarrhythmic evaluation of quinidine, procainamide and lidocaine. Eur. J. Pharmacol. 81, 205–216 (1982).PubMedCrossRefGoogle Scholar
  2. 2.
    Beznák, M.: The effect of the pituitary and growth hormone on the blood pressure and on the ability of the heart to hypertrophy. J. Physiol. 116, 74–83 (1952).PubMedGoogle Scholar
  3. 3.
    Beznák, M.: The effect of different degrees of subdiaphragmatic aortic constriction on heart weight and blood pressure of normal and hypophysectomized rats. Can. J. Biochem. Physiol. 33, 985–994 (1955).PubMedCrossRefGoogle Scholar
  4. 4.
    Dowell, R. T., A. F. Cutilletta, P. C. Sodt: Functional evaluation of the rat heart in situ. J. Appl. Physiol. 39, 1043–1047 (1975).PubMedGoogle Scholar
  5. 5.
    Gerlach, E., B. Deuticke, R. H. Dreisbach: Zum Verhalten von Nucleotiden und ihren dephosphorylierten Abbauprodukten in der Niere bei Ischämie und kurzzeitiger post-ischämischer Wiederdurchblutung. Pflügers Arch. 278, 296–315 (1963).CrossRefGoogle Scholar
  6. 6.
    Gleason, W. L., E. Braunwald: Studies on the first derivative of the ventricular pressure pulse in man. J. Clin. Invest. 41, 80–91 (1962).PubMedCrossRefGoogle Scholar
  7. 7.
    Lee, J. C., S. E. Downing: Ventricular function in norepinephrine-induced cardiomyopathic rabbits. Amer. J. Physiol. 242, H191–H196 (1982).PubMedGoogle Scholar
  8. 8.
    Meerson, F. Z.: Compensatory hyperfunction of the heart and cardiac insufficiency. Circulat. Res. 10, 250–258 (1962).PubMedGoogle Scholar
  9. 9.
    Pfeffer, J. M., M. A. Pfeffer, P. Fletcher, M. C. Fishbein, E. Braunwald: Favorable effects of therapy on cardiac performance in spontaneously hypertensive rats. Amer. J. Physiol. 242, H776–H784 (1982).PubMedGoogle Scholar
  10. 10.
    Rabinowitz, M., R. Zak: Biochemical and cellular changes in cardiac hypertrophy. Ann. Rev. Med. 23, 245–262 (1972).PubMedCrossRefGoogle Scholar
  11. 11.
    Stanton, H. C., G. Brenner, E. D. Mayfield: Studies on isoproterenol-induced cardiomegaly in rats. Amer. Heart J. 177, 72–80 (1969).CrossRefGoogle Scholar
  12. 12.
    Zimmer, H.-G., G. Steinkopff, E. Gerlach: Changes of protein synthesis in the hypertrophying rat heart. Pflügers Arch. 336, 311–325 (1972).PubMedCrossRefGoogle Scholar
  13. 13.
    Zimmer, H.-G., C. Trendelenburg, H. Kammermeier, E. Gerlach: De novo synthesis of myocardial adenine nucleotides in the rat. Acceleration during recovery from oxygen deficiency. Circulat. Res. 32, 635–642 (1973).Google Scholar
  14. 14.
    Zimmer, H.-G., E. Gerlach: Effect of beta-adrenergic stimulation on myocardial adenine nucleotide metabolism. Circulat. Res. 35, 536–543 (1974).PubMedGoogle Scholar
  15. 15.
    Zimmer, H.-G., E. Gerlach: Early metabolic alterations during the development of experimentally induced cardiac hypertrophy. Arzneim.-Forsch./Drug Res. 30(II), Ha, 2001–2007 (1980).Google Scholar
  16. 16.
    Zimmer, H.-G.: Restitution of myocardial adenine nucleotides: acceleration by administration of ribose. J. Physiol., Paris 76, 769–775 (1980).Google Scholar
  17. 17.
    Zimmer, H.-G., H. Ibel, G. Steinkopff, G. Korb: Reduction of the isoproterenol-induced alterations in cardiac adenine nucleotides and morphology by ribose. Science 207, 319–321 (1980).PubMedCrossRefGoogle Scholar
  18. 18.
    Zimmer, H.-G., E. Gerlach: Some metabolic features of the development of experimentally induced cardiac hypertrophy. Europ. Heart J. 3 (Suppl. A), 83–92 (1982).Google Scholar
  19. 19.
    Zimmer, H.-G.: Ribose enhances the isoproterenol-elicited positive inotropic effect in rats in vivo. J. Mol. Cell. Cardiol. 14, 479–482 (1982).PubMedCrossRefGoogle Scholar
  20. 20.
    Zimmer, H.-G.: Measurement of left ventricular hemodynamic parameters in closed-chest rats under control and various pathophysiologic conditions. Basic Res. Cardiol. (in press).Google Scholar

Copyright information

© Dr. Dietrich Steinkopff Verlag, GmbH & Co. KG, Darmstadt 1983

Authors and Affiliations

  • H.-G. Zimmer
    • 1
  1. 1.Physiologisches Institut der UniversitätMünchen 2Germany

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