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Comparative Effects of Ischemia and Hypoxia on Ventricular Relaxation in Isolated Perfused Hearts

  • Carl S. Apstein
  • Laura F. Wexler
  • W. Mark Vogel
  • Ellen O. Weinberg
  • Joanne S. Ingwall

Abstract

Many experimental studies of left ventricular diastolic properties have utilized isolated perfused hearts subjected to either global ischemia or hypoxia. The isolated perfused heart model (see Figure 18-1) has several advantages. The pericardium is removed and the right ventricle is vented; thus, any pericardial or right ventricular interaction effect on left ventricular diastolic relaxation [1–4] is eliminated. Because the imposed ischemic or hypoxic condition is globally distributed throughout the myocardium, regional or segmental differences in contractility are eliminated, thus negating the effects on relaxation of “strong and weak segments in series” [6–7]. For these reasons, the isolated perfused heart model assesses the diastolic properties of the left ventricular chamber consisting of myocytes, connective tissue elements, interstitial fluid, and coronary vasculature.

Keywords

Coronary Flow Global Ischemia Adenosine Infusion Coronary Vasculature Balloon Volume 
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References

  1. 1.
    Glantz SA, Misbach GA, Moores WY, et al (1978). The pericardium substantially affects the left ventricular diastolic pressure-volume relationship in the dog. Circ Res 42: 433–441.PubMedGoogle Scholar
  2. 2.
    Ross J Jr (1979). Acute displacement of the diastolic pressure-volume curve of the left ventricle: Role of the pericardium and the right ventricle. Circulation 59: 32–27.PubMedGoogle Scholar
  3. 3.
    Lorell BH, Palacios I, Daggett WM, et al (1981). Right ventricular distension and left ventricular compliance. Am J Physiol 240: H87 - H98.PubMedGoogle Scholar
  4. 4.
    Maruyama Y, Ashikawa K, Isoyama S, et al (1983). Mechanical interactions between four heart chambers with and without the pericardium in canine hearts. Circ Res 50: 86–100.Google Scholar
  5. 5.
    Waters DD, Da Luz P, Wyatt HL, et al (1977). Early changes in regional and global left ventricular function induced by graded reductions in regional coronary perfusion. Am J Cardiol 39: 537–543.PubMedCrossRefGoogle Scholar
  6. 6.
    Wiegner AW, Allen GJ, Bing OHL (1978). Weak and strong myocardium in series: Implications for segmental dysfunction. Am J Physiol 235: H776 - H783.PubMedGoogle Scholar
  7. 7.
    Brutsaert DL, Rademakers FE, Sys SV (1984). Triple control of relaxation: Implications in cardiac disease. Circulation 69: 190–196.Google Scholar
  8. 8.
    Apstein CS, Deckelbaum L, Mueller M, et al (1977). Graded global ischemia and reperfusion: Cardiac function and lactate metabolism. Circulation 55: 864–872.Google Scholar
  9. 9.
    Apstein CS, Mueller M, Hood WB Jr (1977). Ventricular contracture and compliance changes with global ischemia and reperfusion and their effect on coronary resistance in the rat. Circ Res 41: 206–217.PubMedGoogle Scholar
  10. 10.
    Serizawa T, Vogel WM, Apstein CS, Grossman W (1981). Comparison of acute alterations in left ventricular relaxation and diastolic chamber stiffness induced by hypoxia and ischemia. J Clin Invest 68: 91–102.PubMedCrossRefGoogle Scholar
  11. 11.
    Vogel WM, Apstein CS, Briggs LL, et al (1982). Acute alterations in left ventricular diastolic chamber stiffness: Role of the “erectile” effect of coronary arterial pressure and flow in normal and damaged hearts. Circ Res 51: 465–478.Google Scholar
  12. 12.
    Vogel WM, Briggs LL, Apstein CS (1985). Separation of inherent diastolic myocardial fiber tension and coronary vascular “erectile” contribution to wall stiffness of rabbit hearts damaged by ischemia, hypoxia, calcium paradox and re-perfusion. J Mol Cell Cardiol 17: 57–70.PubMedCrossRefGoogle Scholar
  13. 13.
    Wexler LF, Weinberg EO, Ingwall JS Apstein CS (1986). Acute alterations in diastolic left ventricular chamber distensibility: Mechanistic differences between hypoxemia and ischemia in isolated perfused rabbit and rat hearts. Circ. Res. 59: 515–528.Google Scholar
  14. 14.
    Isoyama S, Lorell BH, Grice WN, et al (1985). Increased diastolic chamber stiffness during simulated angina in isolated hearts. Circulation 72 (suppl III): III - 72.Google Scholar
  15. 15.
    Apstein CS, Grossman W (1987). Opposite initial effects of supply and demand ischemia on left ventricular diastolic compliance: The ischemia-diastolic paradox. J Mol Cell Cardiol 19: 119–128.Google Scholar
  16. 16.
    Salisbury PF, Cross CE, Rieben PA (1960). Influence of coronary artery pressure upon myocardial elasticity. Circ Res 8: 794–800.PubMedGoogle Scholar
  17. 17.
    Bourdillon PD, Poole-Wilson PA (1982). The effects of verapamil, quiescence and cardioplegia on calcium exchange and mechanical function in ischemic rabbit myocardium. Circ Res 50: 360–368.PubMedGoogle Scholar
  18. 18.
    Morgenstern C, Holjes U, Arnold G, Lochner W (1973). The influence of coronary pressure and coronary flow on intracoronary blood volume and geometry of the left ventricle. Pfluegers Arch 340: 101–111.CrossRefGoogle Scholar
  19. 19.
    Olson CO, Attarian EE, Jones RN, et al (1981). The coronary pressure-flow determinants of left ventricular compliance in dogs. Circ Res 49: 856–865.Google Scholar
  20. 20.
    Shine KI, Douglas AM, Ricchiuti N (1976). Ischemia in Isolated ventricular septae: Mechanical events. Am J Physiol 231: 1225–1232.Google Scholar
  21. 21.
    Ingwall JS (1982). Phosphorus nuclear magnetic resonance spectroscopy of cardiac and skeletal muscle. Am J Physiol 242: H729 - H744.PubMedGoogle Scholar
  22. 22.
    Moon RB, Richards H (1973). Determination of intracellular pH as observed by 31P magnetic resonance. J Biol Chem 248: 7276–7278.PubMedGoogle Scholar
  23. 23.
    Garlick PB, Ratta GK, Seely PJ (1979). Studies of acidosis in the ischemic heart by phosphorus nuclear magnetic resonance. Biochem J 184: 547–554.PubMedGoogle Scholar
  24. 24.
    Jacobus WE, Pores IH, Lucas SK, et al (1982). Intracellular acidosis and contractility in the normal and ischemic heart as examined by 31P NMR. J Mol Cell Cardiol 14 (suppl 3): 13–20.PubMedCrossRefGoogle Scholar
  25. 25.
    Wexler LW, Grice WN, Huntington M, et al (1986). Effect of hypertensive coronary perfusion pressure on left ventricular diastolic chamber stiffness. Circulation 74 (suppl II): II - 288 (abstract).Google Scholar
  26. 26.
    Neely JR, Feuvray D (1982). Metabolic products and myocardial ischemia. Am J Pathol 102: 282–291.Google Scholar
  27. 27.
    Rovetto JM, Lamberton WF, Neely JR (1975). Mechanisms of glycolytic inhibition in ischemic rat hearts. Circ Res 37: 742–751.PubMedGoogle Scholar
  28. 28.
    Mathews PM, Radda GK, Taylor DJ (1981). A;P NMR study of metabolism in the hypoxic perfused rat heart. Trans Biochem Soc 9: 23–6237.Google Scholar
  29. 29.
    Flaherty JT, Weisfeldt ML, Bulkley BH, et al (1982). Mechanisms of ischemic myocardial cell damage assessed by phosphorus31 nuclear magnetic resonance. Circulation 65: 561–571.PubMedCrossRefGoogle Scholar
  30. 30.
    Allen DG, Morris PG, Orchard CH (1983). A transient alkalosis precedes acidosis during hypoxia in ferret heart. J Physiol 34: 58–59 P.Google Scholar
  31. 31.
    Tsien RW (1976). Possible effects of hydrogen ions in ischemic myocardium. Circulation 53 (suppl 1): 14–16.Google Scholar
  32. 32.
    Poole-Wilson PA (1978). Measurement of myocardial intracellular pH in pathological states. J Mol Cell Cardiol 10: 511–526.PubMedCrossRefGoogle Scholar
  33. 33.
    Mandel F, Kranias RG, DeGende AG, et al (1982). The effect of pH on the transient state kinetics of Ca’-Mg’ -ATPase of cardiac sarcoplasmic reticulum. Circ Res 50: 310–317.PubMedGoogle Scholar
  34. 34.
    Donaldson SKB, Hermansen L (1978). Differential, direct effects of H+ on Cat+-activated force of skinned fibers from the soleus, cardiac and adductor magnus muscles of rabbits. Pfluegets Arch 376: 55–56.CrossRefGoogle Scholar
  35. 35.
    Fabiato A, Fabiato F (1978). Effects of pH on the myofilaments and the sarcoplasmic reticulum of skinned cells from cardiac and skeletal muscle. J Physiol 276: 233–255.PubMedGoogle Scholar
  36. 36.
    Donaldson SKB, Bond E, Seeger L, et al (1981). Intracellular pH vs Mg ATP2- concentration: Relative importance as determinants of Ca- activated force generation of disrupted rabbit cardiac cells. Cardiovasc Res 15: 268–275.Google Scholar
  37. 37.
    Allen DG, Orchard CH (1983). The effects of changes of pH on intracellular calcium transients in mammalian cardiac muscle. J Physiol 335: 555–567.PubMedGoogle Scholar
  38. 38.
    Allen DG, Eisner DA, Orchard CH (1984). Factors influencing free intracellular calcium concentration in quiescent ferret ventricular muscle. J Physiol 350: 615–630.PubMedGoogle Scholar
  39. 39.
    Lakatta EG, Lappe DL (1981). Diastolic scattered light fluctation, resting force and twitch force in mammalian cardiac muscle. J Physiol 35: 369–394.Google Scholar
  40. 40.
    Matsubara I, Yagi N, Endoh M (1982). The state of cardiac contractile proteins during the diastolic phase. Jpn Circulation J 46: 44–48.CrossRefGoogle Scholar
  41. 41.
    Stern MD, Kort AA, Bhatnagar GM Lakatta EG (1983). Scattered-light intensity fluctuations in diastolic rat cardiac muscle caused by spontaneous Ca-dependent cellular mechanical oscillations. J Gen Physiol 82: 119–153.PubMedCrossRefGoogle Scholar
  42. 42.
    First WH, Palacios I, Powell WH Jr (1978). Effect of hypoxia on myocardial relaxation in isometric cat papillary muscle. J Clin Invest 61: 1218–1224.CrossRefGoogle Scholar
  43. 43.
    Nayler WG, Yopez CE, Poole-Wilson PA (1978). The effect of (3-adrenoreceptor and calcium2+ antagonist drugs on the hypoxiainduced increase in resting tension. Cardiovasc Res 12: 666–674.PubMedCrossRefGoogle Scholar
  44. 44.
    Nayler WG, Poole-Wilson PA, Williams A (1979). Hypoxia and calcium. J Mol Cell Cardiol 11: 683–706.PubMedCrossRefGoogle Scholar
  45. 45.
    Nayler WG, Williams A (1978). Relaxation in heart muscle: Some morphologic and biochemical considerations. Eur J Cardiol 7 (suppl): 35–50.PubMedGoogle Scholar
  46. 46.
    Grossman W, Barry WH (1980). Diastolic pressure-volume relations in the diseased heart. Fed Proc 39: 148–155.PubMedGoogle Scholar
  47. 47.
    Harding DP, Poole-Wilson PA (1980). Calcium exchange in rabbit myocardium during and after hypoxia: Effect of temperature and substrate. Cardiovasc Res 14: 435–445.Google Scholar
  48. 48.
    Greene HL, Weisfeldt ML (1977). Determinants of hypoxic and post-hypoxic myocardial contracture. Am J Physiol 232: 526–533.Google Scholar
  49. 49.
    Bing OHL, Brooks WW, Messer JV (1973). Heart muscle viability following hypoxia: Protective effect of acidosis. Science 180: 1297–1298.Google Scholar
  50. 50.
    Poole-Wilson PA, Lakatta EG, Nayler WG (1977). The effects of acidosis on myocardial function and the uptake of calcium during and after hypoxia. Clin Sci Molec Med 52: 2–3 P.Google Scholar
  51. 51.
    Dwyer EM (1970). Left ventricular pressure-volume alterations and regional disorders of contraction during myocardial ischemia induced by atrial pacing. Circulation 42: 1111–1122.PubMedGoogle Scholar
  52. 52.
    McLaurin LP, Rolett SL, Grossman W (1973). Impaired left ventricular relaxation during pacing induced ischemia. Am J Cardiol 32: 751–757.PubMedCrossRefGoogle Scholar
  53. 53.
    Barry WH, Brooker JZ, Alderman EL, Harrison DC (1974). Changes in diastolic stiffness and tone of the left ventricle during angina pectoris. Circulation 49: 255–263.PubMedGoogle Scholar
  54. 54.
    Mann T, Brodie BR, Grossman W, McLaurin LP (1977). Effects of angina on the left ventricular diastolic pressure volume relationship. Circulation 55: 761–766.PubMedGoogle Scholar
  55. 55.
    Mann T, Goldberg S, Mudge GH Jr, Grossman W (1979). Factors contributing to altered left ventricular diastolic properties during angina pectoria. Circulation 52: 14–20.Google Scholar
  56. 56.
    Serizawa T, Carabello BA, Grossman W (1980). Effect of pacing induced ischemia on left ventricular diastolic pressure-volume relations in dogs with coronary stenoses. Circ Res 46: 430–439.PubMedGoogle Scholar
  57. 57.
    Bourdillon PD, Lorell BH, Mirsky I, et al (1983). Increased regional myocardial stiffness of the left ventricle during pacing-induced angina in man. Circulation 67: 316–323.PubMedCrossRefGoogle Scholar
  58. 58.
    Tennant R, Wiggers CJ (1985). Effect of coronary occulsion on myocardial contraction. Am J Physiol 112: 351–361.Google Scholar
  59. 59.
    Forrester JS, Diamond G, Parmley WE, Swan HJC (1972). Early increase in left ventricular compliance after infarction. J Clin Invest 51: 598–603.PubMedCrossRefGoogle Scholar
  60. 60.
    Theroux P, Franklin D, Ross J Jr, Kemper WS (1974). Regional myocardial function during acute coronary artery occlusion and its modification by pharmacologic agents in the dog. Circ Res 35: 825–908.Google Scholar
  61. 61.
    Theroux P, Ross J Jr, Franklin D, et al (1977). Regional myocardial function and dimensions early and late after myocardial infarction in the unanaesthetized dog. Circ Res 40: 158–165.PubMedGoogle Scholar
  62. 62.
    Tyberg JV, Forrester JS, Wyatt HL, et al (1974). An analysis of segmental ischemic dysfunction utilizing the pressure length loop. Circulation 49: 748–754.PubMedGoogle Scholar
  63. 63.
    Pirzada FA, Ekong EA, Vokonas PS, et al (1976). Experimental myocardial infarction. XIII. Sequential changes in left ventricular pressure-length relationship in the acute phase. Circulation 53: 970–974.Google Scholar
  64. 64.
    Vokonas PS, Pirzada FA, Hood WB Jr (1976). Experimental myocardial infarction. XII. Dynamic changes in sequential mechanical behavior of infarcted and non-infarced myocardium. Am J Cardiol 37: 853–859.Google Scholar
  65. 65.
    Weiner JM, Apstein CS, Arthur JH, et al (1976). Persistence of myocardial injury following brief periods of coronary occlusion. Cardiovasc Res 10: 678–686.PubMedCrossRefGoogle Scholar
  66. 66.
    Hess OM, Osakada G, Lavelle JF, et al (1983). Diastolic myocardial wall stiffness and ventricular relaxation during partial and complete coronary occlusions in the conscious dog. Circ Res 52: 387–400.PubMedGoogle Scholar
  67. 67.
    Reagan TJ, Effros RM, Haider B, et al (1976) Myocardial ischemia and cell acidosis: Modification by alkali and the effects on ventricular function and cation composition. Am J Cardiol 37: 501–507.Google Scholar
  68. 68.
    Cobbe SM, Poole-Wilson PA (1980). The time of onset and severity of acidosis in myocardial ischemia. J Mol Cell Cardiol 12: 745–760.PubMedCrossRefGoogle Scholar
  69. 69.
    Momomura S, Ingwall JS, Parker JA, et al (1985). The relationships of high energy phosphates, tissue pH, and regional blood flow to diastolic distensibility in the ischemic dog myocardium. Circ. Res. 57: 822–835.Google Scholar
  70. 70.
    Apstein CS, Deckelbaum L, Hagopian L, Hood WB Jr (1978). Acute cardiac ischemia and re-perfusion. Contractility, relaxation and glycolysis. Am J Physiol 235: H637 - H648.PubMedGoogle Scholar
  71. 71.
    Bricknell OL, Daries PS, Opie LH (1981). A relationship between adenosine triphosphate, glyocolysis and ischemic contracture in the isolated rat heart. J Mol Cell Cardiol 13: 941–945.PubMedCrossRefGoogle Scholar
  72. 72.
    Gudbjarnson S, Mathes P, Raven KG (1970). Functional compartmentation of ATP and creatine phosphate in heart muscle. J Mol Cell Cardiol 1: 325–339.CrossRefGoogle Scholar
  73. 73.
    Shrago E, Shug AL, Sul H, et al (1976). Control of energy production in myocardial ischemia. Circ Res 38(Suppl 1 ): 17 5–79.Google Scholar

Copyright information

© Martinus Nijhoff Publishing 1987

Authors and Affiliations

  • Carl S. Apstein
  • Laura F. Wexler
  • W. Mark Vogel
  • Ellen O. Weinberg
  • Joanne S. Ingwall

There are no affiliations available

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