Advertisement

Coronary Perfusion as the Major Determinant of Myocardial Contractility in the Heart: Implication for Myocardial Hibernation

  • Masafumi Kitakaze
Chapter
  • 43 Downloads
Part of the Developments in Cardiovascular Medicine book series (DICM, volume 194)

Abstract

Coronary perfusion pressure and blood flow are closely linked to myocardial metabolic states and contractility. When coronary perfusion pressure decreases below the level of the coronary flow autoregulation, myocardial contractility is markedly decreased. Myocardial ischemia causes accumulation of H+ and inorganic phosphates, both of which decrease the myofilament sensitivity to Ca2+ and maximal response of myofilaments to Ca2+. Furthermore, adenosine and EDRF (NO), produced during ischemia, stimulate adenylate and guanulate cyclase, respectively, both of which have been reported to decrease myocardial contractility. In turn, norepinephrine is released according to the severity of myocardial ischemia, which tends to compensate the depression of myocardial contractility. On the other hand, when myocardial ischemia is not apparent due to coronary flow autoregulation during mild reduction of coronary perfusion pressure, myocardial contractility decreases, recognized as Gregg ’s phenomenon. There are several hypotheses to explain this phenomenon: 1) decreases in sarcomere length of the myofilaments, 2) reversal of latent myocardial ischemia, 3) release of cardiodepressive agents, and 4) decreases in either Ca2+ transient or Ca2+ sensitivity. Ca2+ transients were measured in the ferret Langendorff preparation at various perfusion pressure; the amplitude of Ca2+ transients was decreased when coronary perfusion pressure was reduced in the range of coronary flow autoregulation. Taken together, these results support the hypothesis of the tight linkage between coronary perfusion and myocardial contractility in normal and ischemic hearts. The concert interaction between myocardial perfusion and intracellular Ca2+ concentration may be essential for maintaining homeostasis of myocardial cellular function.

Keywords

Perfusion Pressure Coronary Blood Flow Myocardial Contractility Reactive Hyperemia Coronary Perfusion 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Chang AE, Detar R. Oxygen and vascular smooth muscle contraction revisited. Am J Physiol 1980;238:H716–H718.PubMedGoogle Scholar
  2. 2.
    Case RB, Felix A, Wachter M et al. Relative effect of CO2 on canine coronary vascular resistance. Circ Res 1978;42:410–418.PubMedCrossRefGoogle Scholar
  3. 3.
    Broten TP, Feigl EO. Role of myocardial oxygen and carbon dioxide in coronary autoregulation. Am J Physiol 1992;262:H1231–H1237.PubMedGoogle Scholar
  4. 4.
    Hori M, Kitakaze M. Adenosine, the heart, and coronary circulation. Hypertension 1991:18:565–574.PubMedCrossRefGoogle Scholar
  5. 5.
    Berne RM, Rubio R, Cumish RR. Release of adenosine from ischemic brain: Effect on cerebral vascular resistance and incorporation into cerebral adenine nucleotides. Circ Res 1974;35:262–271.CrossRefGoogle Scholar
  6. 6.
    Schrader J, Haddy FJ, Gerlach E. Release of adenosine, inosine and hypoxanthine from the isolated guinea pig heart during hypoxia, flow-autoregulation and reactive hyperemia. Pflugers Arch 1977;369:l–6.Google Scholar
  7. 7.
    Kroll K, Feigl EO. Adenosine is unimportant in controlling coronary blood flow in unstressed dog hearts. Am J Physiol 1985;249:H1186–H1187.Google Scholar
  8. 8.
    Dole WP, Yamada N, Bishop VS et al. Role of adenosine in coronary blood flow regulation after reductions in perfusion pressure. Circ Res 1985;56:517–524.PubMedCrossRefGoogle Scholar
  9. 9.
    Gidday JM, Ely SW, Esther JW et al. Progressive attenuation of coronary reactive hyperemia with increasing interstitial theophylline permeation. Fed Proc 1984;43:1084.Google Scholar
  10. 10.
    Morioka T, Kitakaze M, Minamino T et al. Role of endogenous adenosine in coronary pressure-flow relationship in dogs. J. Am. Coll. Cardiol. Special Issue 1994;262A.Google Scholar
  11. 11.
    Ueeda M, Silvia S, Olsson RA. Nitric oxide modulates coronary autoregulation in the guinea pig. Circ Res 1992;70:1296–1303.PubMedCrossRefGoogle Scholar
  12. 12.
    Kitakaze M, Takashima S, Node K et al. Role of nitric oxide for regulation of coronary blood flow of ischemic myocardium in dogs. Am. J. Coll. Cardiol. (in press).Google Scholar
  13. 13.
    Daut J, Maier-Rudolph W, von Beckerath N et al. Hypoxic dilation of coronary arteries is mediated by ATP-sensitive potassium channels. Science 1990;247:1341–1344.PubMedCrossRefGoogle Scholar
  14. 14.
    Komaru T, Lamping KG, Easthan CL et al. Role of ATP-sensitive potassium channels in coronary microvascular autoregulatory responses. Circ Res 1991; 69:1146–1151.PubMedCrossRefGoogle Scholar
  15. 15.
    Aversano T, Ouyang P, Silverman H. Blockade of the ATP-sensitive potassium channel modulate reactive hyperemia in the canine coronary circulation. Circ Res 1991;69:618–622.PubMedCrossRefGoogle Scholar
  16. 16.
    Kuo L, Davis MJ, Chilian WM. Myogenic activity in isolated subepicardial and subendocardial coronary arteries. Am J Physiol 1988;255:H1558–H1562.PubMedGoogle Scholar
  17. 17.
    Zuberbuhler RC, Bohr DF. Responses of coronary smooth muscle to catecholamine. Circ Res 1965;16:431–440.PubMedCrossRefGoogle Scholar
  18. 18.
    Buffington CW, Feigl EO. Effect of coronary artery pressure on transmural distribution of adrenergic coronary vasoconstriction in the dog. Circ Res 1983;53:613–621.PubMedCrossRefGoogle Scholar
  19. 19.
    Kitakaze M, Hori M, Tamai J et al. al-Adrenoceptor activity regulates release of adenosine from the ischemic myocardium in dogs. Circ Res 1987;60:631–639.PubMedCrossRefGoogle Scholar
  20. 20.
    Buxton ILO, Walther J, Westfall DP. Purinergic mechanisms in cardiac blood vessels: Stimulation of endothelial cell a receptors in vitro by the neurotransmitter norepinephrine leads to the rapid release of ATP and its subsequent breakdown to adenosine (abstract). Heart and Vessel 1990;4(Suppl):27.Google Scholar
  21. 21.
    Kitakaze M, Hori M, Morioka T, et. al-adrenoceptor activation increases ectosolic 5’-nucleotidase activity and adenosine release in rat cardiomyocytes by activing protein kinase C. Circulation 91:2226–2234,1995PubMedCrossRefGoogle Scholar
  22. 22.
    Kitakaze M, Hori M, Kamada T. Role of adenosine and its interaction with alpha adrenoceptor activity in ischemic and reperfusion injury of the myocardium. Cardiovasc Res 1993;27:18–27.PubMedCrossRefGoogle Scholar
  23. 23.
    Gregg DE. Effects of coronary perfusion pressure or or coronary flow on oxygen usage of the myocardium. Circ Res 1963;13:497–500.PubMedCrossRefGoogle Scholar
  24. 24.
    Kitakaze M, Marban E. Cellular mechanism of the modulation of contractile function by coronary perfusion pressure in ferret hearts. J Physiol 1989;414:455–472.PubMedGoogle Scholar
  25. 25.
    Schouten VJ, Allaart CP, Westerhof N. Effect of perfusion pressure on force contraction in thin papillary muscles and trabeculae from rat heart. J Physiol 1992;451:585–604.PubMedGoogle Scholar
  26. 26.
    Feigl EO. Coronary physiology. Physiol Rev 1983;63:l–205.Google Scholar
  27. 27.
    Haneda T, Morgan HE, Watson PA. Effect of calcium uptake increased by elevated aortic pressure on total and ribosomal protein synthesis in rat heart. J Mol Cell Cardiol 1988;20:Suppl(III)-S35.Google Scholar
  28. 28.
    Rahimtoola SH, Griffith GC. The hibernating myocardium. Am Heart J 1989;117:211–221.PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media New York 1997

Authors and Affiliations

  • Masafumi Kitakaze

There are no affiliations available

Personalised recommendations