Advertisement

Pathophysiological Behavior of the Myocardium in Acute Ischemia and Reperfusion, with Special Emphasis on the Sarcoplasmic Reticulum

  • Takashi Katagiri
  • Eiichi Geshi
  • Hirohisa Arata
  • Haruhiko Ishioka
  • Seiji Itoh
  • Noburu Konno
Part of the Progress in Experimental Cardiology book series (PREC, volume 1)

Abstract

The myocardium under severe ischemia and reperfusion exhibits four types of different pathophysiologic behaviors: coagulation necrosis, stunning, ischemic preconditioning, and reperfusion injury. This chapter describes these changes in the postischemic myocardium in relation to the length of ischemia. Canine hearts were made ischemic by occludmg the left anterior descending coronary artery (LAD), and the sarcoplasmic reticulum (SR) from the ischemia-reperfused myocardium was analyzed. In permanent occlusion of the LAD, Ca2+-ATPase activity of the SR was reduced simultaneously with the degradation of the major ATPase protein in ischemia for 20 to 30 minutes. In the stunned myocardium, with occlusion of the LAD for 15 minutes and reperfusion, long-term reduction in the activity of the SR was noted simultaneously with a reduction in the percent of segment shortening, but without degradation of the ATPase protein of the SR. In the preconditioned myocardium, in which the LAD was occluded four times for five minutes each prior to LAD occlusion for 60 minutes and reperfusion, both ATPase activity and the SR ATPase protein were preserved In reperfusion of the LAD after occlusion for 10 to 30 minutes, reduction in Ca2+-ATPase activity and degradation of the ATPase protein occurred earlier, simultaneously with generation of free radicals, suggesting reperfusion injury. We conclude that pathophysiologic behaviors of the postischemic myocardium proceed in quite different ways depending upon the length of ischemia and will only be fully understood in the light of studies on ischemia and reperfusion of the heart muscle.

Keywords

Electron Spin Resonance ATPase Activity Sarcoplasmic Reticulum Left Anterior Descend Electron Spin Resonance Signal 
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.
    Blumgart HL, Gilligan DR, Schlesinger MJ. 1941. Experimental studies on the effect of temporary occlusion of coronary arteries. II. The production of myocardial infarction. Am Heart J 22:374–389.CrossRefGoogle Scholar
  2. 2.
    Jennings RB, Ganote CE. 1974. Structural changes in myocardium during acute ischemia. Circ Res 34, 35 (Suppl III):III-1456–III-168.Google Scholar
  3. 3.
    Braunwald E, Kloner RA. 1982. The stunned myocardium: prolonged, postischemic ventricular dysfunction. Circulation 66:1146–1149.PubMedGoogle Scholar
  4. 4.
    Murry CE, Jennings RB, Reimer KA. 1986. Preconditioning with ischemia: a delay of lethal injury in ischemic myocardium. Circulation 74:1124–1136.PubMedGoogle Scholar
  5. 5.
    Braunwald E, Kloner RA. 1985. Myocardial reperfusion: a double edged sword? J Clin Invest 76:1713–1719.PubMedCrossRefGoogle Scholar
  6. 6.
    Konno N, Yanagishita T, Geshi E, Katagiri T. 1987. Degradation of the cardiac sarcoplasmic reticulum in acute myocardial ischemia. Jpn Circ J 51:411–420.PubMedGoogle Scholar
  7. 7.
    Bolli R, Pate1 BS, Jeroudi MO, Lai EK, McCay PB. 1988. Demonstration of free radical generation in “stunned” myocardium of intact dogs with the use of the spin trap α-phenyl N-tert-butyl nitrone. J Clin Invest 82:476–485.PubMedGoogle Scholar
  8. 8.
    Itoh S, Yanagishita T, Mukae S, Konno N, Katagiri T. 1992. Study on reperfusion injury on sarcoplasmic reticulum in acute myocardial ischemia. Jpn Circ J 56:411–420.Google Scholar
  9. 9.
    Arata H, Geshi E, Ishioka H, Katagiri T. 1995. Alterations in sarcoplasmic reticulum and mitochondrial functions in stunned myocardium: relation between regional myocardial function and biochemical analyses. Showa Univ J Med Sci 7:83–94.Google Scholar
  10. 10.
    Bolli R. 1990. Mechanism of myocardial “stunning”. Circulation 82:723–738.PubMedGoogle Scholar
  11. 11.
    Murry CE, Richard VJ. 1991. Myocardial protection is lost before contractile function recovers from ischemic preconditioning. Am J Physiol 260:H796–H804.PubMedGoogle Scholar
  12. 12.
    Liu GS, Thronton J, Van Winkle DM, Stanley AWH, Olsson RA, Downey JM. 1991. Protection against infarction afforded by preconditioning is mediated by A1 adenosine receptors in rabbit heart. Circulation 84:350–356.PubMedGoogle Scholar
  13. 13.
    Murry CE, Jennings RB, Reimer KA. 1991. New insights into potential mechanisms of ischemic preconditioning. Circulation 84:442–445.PubMedGoogle Scholar
  14. 14.
    McCord JM. 1985. Oxygen-derived free radicals in postischemic tissue injury. N End J Med 312:159–163.CrossRefGoogle Scholar

Copyright information

© Kluwer Academic Publishers 1998

Authors and Affiliations

  • Takashi Katagiri
    • 1
  • Eiichi Geshi
    • 1
  • Hirohisa Arata
    • 1
  • Haruhiko Ishioka
    • 1
  • Seiji Itoh
    • 1
  • Noburu Konno
    • 1
  1. 1.Showa University School of MedicineJapan

Personalised recommendations