Chronic Changes in the Canine Myocardium After Coronary Microembolization

  • Masatsugu Hori
  • Yukihiro Koretsune
  • Kunimitsu Iwai
  • Koichi Goto
  • Hiroshi Sato
  • Katsuomi Iwakura
  • Akira Kitabatake
  • Takenobu Kamada


Recently, there has been interest in acute microcirculatory abnormalities of the coronary arteries, particularly microembolism, as a primary cause of or secondary outcome of the no-reflow phenomenon following recanalization of occluded coronary arteries [1, 2]. It is reported that interruption of the coronary blood flow for more than 30 min produces an incomplete return of blood flow after reperfusion [1], and the area of no-reflow increases with the duration of ischemia [3]. Recanalization of occluded arteries is often observed in the clinical setting either spontaneously or after coronary thrombolytic therapy (PTCR) in patients with acute myocardial infarction. The heart reperfused after a certain time-lag may have regional impairment of coronary perfusion, presumably’ at the level of the capillaries or feeding arterioles. Several mechanisms for the noreflow phenomenon have been suggested. Capillary compression by parenchymal cell swelling [2] or interstitial edema [4], obstruction by endothelial cell swelling [5], thrombosis [6], erythrocyte impaction [7], leukocyte plugging [8], and platelet aggregates [9] have been reported as a cause of the perfusion impedance after reperfusion. Although it has been claimed in several studies that plugging of the blood cells in the microvasculature may not be a primary cause of noreflow [10, 11], entrapment of blood cells secondary to the microcirculatory disturbance could further impede the flow and delay the recovery of ischemia. Prolonged myocardial stunning often observed following reperfusion might be attributed in part to this microcirculatory abnormality. We have previously demonstrated a characteristic hyperemic flow response of coronary blood flow after coronary embolization of microspheres, which mimic blood cell plugging [12]. In this chapter, we shall discuss the chronic changes in coronary blood flow and functional and histological changes in the embolized myocardium.


Coronary Blood Flow Hyperemic Response Left Circumflex Coronary Artery Canine Myocardium Rapid Atrial Pace 
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  1. 1.
    Krug A, De Rochemont WM, Krob G (1966) Blood supply of the myocardium after temporary coronary occlusion. Circ Res 19: 57PubMedGoogle Scholar
  2. 2.
    Kloner RA, Ganote CE, Jennings RB (1974) The “no-reflow” phenomenon after temporary coronary occlusion in the dog. J Clin Invest 54: 1496PubMedCrossRefGoogle Scholar
  3. 3.
    Darsee JR, Kloner RA (1980) The no reflow phenomenon: A time limited factor for reperfusion after coronary occlusion? Am J Cardiol 46: 800CrossRefGoogle Scholar
  4. 4.
    Reimer KA, Jennings RB (1979) The changing anatomic reference base of evolving myocardial infarction. Underestimation of myocardial collateral blood flow and overestimation of experimental anatomic infarct size due to tissue edema, hemorrhage and acute inflammation. Circulation 60: 866PubMedGoogle Scholar
  5. 5.
    Armiger LC, Gavin JB (1975) Changes in the microvasculature of ischemic and infarcted myocardium. Lab Invest 33: 51PubMedGoogle Scholar
  6. 6.
    Ruegsegger P, Nydick I, Abarquez F, Cliffton EF, La Due JS (1960) Effect of fibrinolytic (plasmin) therapy on the physiopathology of myocardial infarction. Am J Cardiol 6: 519PubMedCrossRefGoogle Scholar
  7. 7.
    Gavin JB, Nevalainen TJ, Seelye RN, Webster V, Thomson RW (1978) An association between the onset of rigor and loss of vascular competence in early myocardial infarcts. Pathology 10: 219PubMedCrossRefGoogle Scholar
  8. 8.
    Engler RL, Schmid-Schoebein GW, Pavelec RS (1983) Leukocyte capillary plugging in myocardial ischemia and reperfusion in the dog. Am J Pathol 111: 98PubMedGoogle Scholar
  9. 9.
    Schneider MD (1980) Role of the blood platelet in the pathogenesis and complications of experimental myocardial ischemia. Am J Vet Res 45: 451Google Scholar
  10. 10.
    Nevalainen TJ, Gavin JB, Seelye RN, Whitehouse S, Donnell M (1978) The effect of rigor mortis on the passage of erythrocytes and fluid through the myocardium of the isolated dog hearts. Pathology 10: 227PubMedCrossRefGoogle Scholar
  11. 11.
    Humphrey SM, Gavin JB, Herdson PB (1980) The relationship of ischemic contracture to vascular reperfusion in the isolated rat heart. J Moll Cell Cardiol 12: 1397CrossRefGoogle Scholar
  12. 12.
    Hori M, Inoue M, Kitakaze M, Koretsune Y, Iwai K, Tarnai J, Ito H, Kitabatake A, Sato T, Kamada T (1986) Role of adenosine in hyperemic response of coronary blood flow in microembolization. Am J Physiol 250: H509–H518PubMedGoogle Scholar
  13. 13.
    Bing RJA, Castellanos E, Grandel C, Luptun C, Siegel A (1956) Experimental myocardial infarction: circulatory, biochemical and pathologic changes. Am J Med Sci 232: 533PubMedCrossRefGoogle Scholar
  14. 14.
    West JW, Kobayashi T, Anderson FS (1972) Effect of coronary embolization on coronary blood flow and coronary sinus venous blood oxygen saturation in dogs. Circ Res 10: 722Google Scholar
  15. 15.
    Hori M, Koretsune Y, Iwai K, Kitakaze M, Tarnai J, Kitabatake A, Inoue M, Kamada T (1987) A possible model of the anginal syndrome with normal coronary arteriograms: Microembolization of canine coronary arteries. Heart Vessels 3: 7PubMedCrossRefGoogle Scholar
  16. 16.
    Munro G, Ba1chum OJ, Owens JC, Swan H (1956) Experimental chronic myocardial insufficiency produced by coronary embolization. Surg Forum 6: 204PubMedGoogle Scholar
  17. 17.
    Smiseth OA, Lindal S, Mjos OD, Vik-mo H, Jorgensen L (1983) Progression of myocardial damage following coronary microembolization in dogs. Acta Path Microbioi Immunol Scand Sect A 91: 115Google Scholar
  18. 18.
    Eng C, Cho S, Factor SM, Sonnenblick EH, Kirk ES (1984) Myocardial macronecrosis produced by micros ph ere embolization: Role of an alpha-adrenergic tonic influence on the coronary microcirculation. Circ Res 54: 74PubMedGoogle Scholar
  19. 19.
    Weber KT, Malinin TI, Dennison BH, Faqua JM, Speaker DM, Hastings FW (1972) Experimental myocardial ischemia and infarction: Production of diffuse myocardial lesions in unanesthetized calves. Am J Cardiol 29: 793PubMedCrossRefGoogle Scholar
  20. 20.
    Mukherjee A, Bush LR, McCoy KE, Duke RJ, Hagler H, Maxilian Buya L, Willerson JT (1982) Relationship between beta-adrenergic receptor numbers and physiological responses during experimental canine myocardial ischemia. Circ Res 50: 735PubMedGoogle Scholar
  21. 21.
    Karliner JS, Stevens M, Grattan M, Woloszyn W, Honbo N, Hoffman HE (1986) Beta-adrenergic receptor properties of canine myocardium: Effect of chronic myocardial infarction. J Am Coll Cardiol 8: 349PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Tokyo 1988

Authors and Affiliations

  • Masatsugu Hori
  • Yukihiro Koretsune
  • Kunimitsu Iwai
  • Koichi Goto
  • Hiroshi Sato
  • Katsuomi Iwakura
  • Akira Kitabatake
  • Takenobu Kamada
    • 1
  1. 1.The First Department of MedicineOsaka University School of MedicineFukushima-ku, Osaka, 553Japan

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