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Cardiac Remodeling and Failure pp 205–230Cite as

Alterations in Hemodynamic and Neurohumoral Responses to Exercise in Swine with Left Ventricular Remodeling Early after Myocardial Infarction: Role of Blunted NO Bioavailability

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Part of the book series: Progress in Experimental Cardiology ((PREC,volume 5))

Abstract

Flow reserve and NO bioavailability are blunted in the surviving hypertrophied left ventricle (LV) early after myocardial infarction (MI). During exercise, exacerbation of hemodynamic abnormalities, neurohumoral activation and perturbed NO bioavailability could exhaust coronary flow reserve and thereby impair myocardial O2 supply. We tested this hypothesis in swine with a 2–3 week old myocardial infarction (MI) and determined whether a loss of NO bioavailability contributes to impaired tissue perfusion during exercise.

Under resting conditions, Swine with a MI had a lower cardiac output (20%), stroke volume (28%), LVdP/dtmax (18%), systemic (22%) and pulmonary (19%) vascular conductance, and increased left atrial (225%) and pulmonary artery (75%) pressures, compared to normal swine. Systemic and coronary vasodilator responses to ATP, but not nitroprusside, were blunted in swine with MI. In MI swine, the exercise-induced increases in cardiac pump function were blunted compared to normals. Exercise-induced increases in plasma norepinephrine and endothelin levels were exacerbated and while relative sympathetic drive was maintained, cardiac responsiveness to norepinephrine was attenuated in MI swine. In addition, the exercise-induced resembling the vasodilator responses in normal swine following blockade of NO synthase with Nω-nitro-L-arginine (NLA, 20mg/kg iv). However, NLA resulted in similar degrees of systemic and pulmonary vasoconstriction in normal and MI swine, both under resting conditions and during treadmill exercise. Selective inhibition of iNOS with aminoguanidine (20mg/kg iv) had no effect on vascular tone in MI either at rest or during exercise. Despite lower capillary densities in the hypertrophied non-infarcted LV and despite subendocardial hypoperfusion (relative to subepicardial perfusion) during exercise, which necessitated a slight increase in O2-extraction, there was no metabolic evidence of overt myocardial ischemia during exercise as indicated by the arterio-coronary venous pH difference. The perturbation in myocardial O2-balance was not caused by a loss of NO availability.

In conclusion, LV dysfunction, neurohumoral activation and blunted systemic, pulmonary and coronary vasodilation are present in exercising swine with a 2–3-week-old infarction. However, although agonist-induced vasodilation is already impaired early after MI, the contribution of endothelial NO synthase-derived NO to regulation of vascular tone under basal conditions and during exercise is maintained.

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References

  1. Karam R, Healy BP, Wicker P. 1990. Coronary reserve is depressed in postmyocardial infarction reactive cardiac hypertrophy. Circulation 81:238–246.

    Article  PubMed  CAS  Google Scholar 

  2. Kalkman EA, Bilgin YM, van Haren P, van Suylen RJ, Saxena PR, Schoemaker RG. 1996. Determinants of coronary reserve in rats subjected to coronary artery ligation or aortic banding. Cardiovasc Res 32:1088–1095.

    Article  PubMed  CAS  Google Scholar 

  3. Zhang J, Wilke N, Wang Y, Zhang Y, Wang C, Eijgelshoven MH, Cho YK, Murakami Y, Ugurbil K, Bache RJ, From AH. 1996. Functional and bioenergetic consequences of postinfarction left ventricular remodeling in a new porcine model. MRI and 31 P-MRS study. Circulation 94:1089–1100.

    Article  PubMed  CAS  Google Scholar 

  4. Duncker DJ, Stubenitsky R, Tonino PA, Verdouw PD. 2000. Nitric oxide contributes to the regulation of vasomotor tone but does not modulate O2-consumption in exercising swine. Cardiovasc Res 47:738–748.

    Article  PubMed  CAS  Google Scholar 

  5. Kiowski W, Sutsch G, Schalcher C, Brunner HP, Oechslin E. 1998. Endothelial control of vascular tone in chronic heart failure. J Cardiovasc Pharmacol 32:S67–73.

    PubMed  CAS  Google Scholar 

  6. Recchia FA, McConnell PI, Bernstein RD, Vogel TR, Xu X, Hintze TH. 1998. Reduced nitric oxide production and altered myocardial metabolism during the decompensation of pacing-induced heart failure in the conscious dog. Circ Res 83:969–979.

    Article  PubMed  CAS  Google Scholar 

  7. Wang J, Seyedi N, Xu XB, Wolin MS, Hintze TH. 1994. Defective endothelium-mediated control of coronary circulation in conscious dogs after heart failure. Am J Physiol 266:H670–680.

    PubMed  CAS  Google Scholar 

  8. Haitsma DB, Bac D, Raja N, Boomsma F, Verdouw PD, Duncker DJ. 2001. Minimal impairment of myocardial blood flow responses to exercise in the remodeled left ventricle early after myocardial infarction, despite significant hemodynamic and neurohumoral alterations. Cardiovasc Res 52:471–428.

    Article  Google Scholar 

  9. Haitsma DB, Merkus D, Vermeulen J, Verdouw PD, Duncker DJ. 2002. Nitric oxide production is maintained in exercising swine with chronic left ventricular dysfunction. Am J Physiol 282:H2198–H2209.

    CAS  Google Scholar 

  10. Drexler H, Kastner S, Strobel A, Studer R, Brodde OE, Hasenfuss G. 1998. Expression, activity and functional significance of inducible nitric oxide synthase in the failing human heart. J Am Coll Cardiol 32:955–963.

    Article  PubMed  CAS  Google Scholar 

  11. Van der Giessen WJ, Van Woerkens LJ, Duncker DJ, Roelandt JR, Verdouw PD. 1989. Acute hemodynamic effects of nisoldipine and pimobendan in conscious pigs with chronic heart failure. J Cardiovasc Pharmacol 14:653–658.

    Article  Google Scholar 

  12. Duncker DJ, Haitsma DB, van der Geest IE, Stubenitsky R, Van Meegen JR, Manin’t Veld AJ, Verdouw PD. 1997. Systemic, pulmonary and coronary haemodynamic actions of the novel dopamine receptor agonist Z1046 in awake pigs at rest and during treadmill exercise. Br J Pharmacol 120:1101–1113.

    Article  PubMed  CAS  Google Scholar 

  13. Duncker DJ, Stubenitsky R, Verdouw PD. 1998. Autonomic control of vasomotion in the porcine coronary circulation during treadmill exercise: evidence for feed-forward beta-adrenergic control. Circ Res 82:1312–1322.

    Article  PubMed  CAS  Google Scholar 

  14. Van Kats JP, Duncker DJ, Haitsma DB, Schuijt MP, Niebuur R, Stubenitsky R, Boomsma F, Schalekamp MA, Verdouw PD, Danser AH. 2000. Angiotensin-Converting enzyme inhibition and angiotensin II type 1 receptor blockade prevent cardiac remodeling in pigs after myocardial infarction: role of tissue angiotensin II. Circulation 102:1556–1563.

    Article  Google Scholar 

  15. Wolff DJ, Lubeskie A, Gauld DS, Neulander MJ. 1998. Inactivation of nitric oxide synthases and cellular nitric oxide formation by N6-iminoethyl-L-lysine and N5-iminoethyl-L-ornithine. Eur J Pharmacol 350:325–334.

    Article  PubMed  CAS  Google Scholar 

  16. Boer R, Ulrich WR, Klein T, Mirau B, Haas S, Baur I. 2000. The inhibitory potency and selectivity of arginine substrate site nitric-oxide synthase inhibitors is solely determined by their affinity toward the different isoenzymes. Mol Pharmacol 58:1026–1034.

    PubMed  CAS  Google Scholar 

  17. Yoshida T, Engelman RM, Engelman DT, Rousou JA, Maulik N, Sato M, Elliott GT, Das DK. 2000. Preconditioning of swine heart with monophosphoryl lipid A improves myocardial preservation. Ann Thorac Surg 70:895–900.

    Article  PubMed  CAS  Google Scholar 

  18. Schaper W, Remijsen P, Xhonneux R. 1969. The size of myocardial infarction after experimental coronary artery ligation. Z Kreislaufforsch 58:904–909.

    PubMed  CAS  Google Scholar 

  19. Armstrong PW, Stopps TP, Ford SE, de Bold AJ. 1986. Rapid ventricular pacing in the dog: pathophysiologic studies of heart failure. Circulation 74:1075–1084.

    Article  PubMed  CAS  Google Scholar 

  20. Spinale FG, Fulbright BM, Mukherjee R, Tanaka R, Hu J, Crawford FA, Zile MR. 1992. Relation between ventricular and myocyte function with tachycardia-induced cardiomyopathy. Circ Res 71:174–187.

    Article  PubMed  CAS  Google Scholar 

  21. Spinale FG, de Gasparo M, Whitebread S, Hebbar L, Clair MJ, Melton DM, Krombach RS, Mukherjee R, Iannini JP, O SJ. 1997. Modulation of the renin-angiotensin pathway through enzyme inhibition and specific receptor blockade in pacing-induced heart failure: I. Effects on left ventricular performance and neurohormonal systems. Circulation 96:2385–2396.

    Article  PubMed  CAS  Google Scholar 

  22. Traverse JH, Melchert P, Pierpont GL, Jones B, Crampton M, Bache RJ. 1999. Regulation of myocardial blood flow by oxygen consumption is maintained in the failing heart during exercise. Circ Res 84:401–408.

    Article  PubMed  CAS  Google Scholar 

  23. Drexler H, Toggart EJ, Glick MR, Heald J, Flaim SF, Zelis R. 1986. Regional vascular adjustments during recovery from myocardial infarction in rats. J Am Coll Cardiol 8:134–142.

    Article  PubMed  CAS  Google Scholar 

  24. Drexler H, Lu W. 1992. Endothelial dysfunction of hindquarter resistance vessels in experimental heart failure. Am J Physiol 262:H1640–1645.

    PubMed  CAS  Google Scholar 

  25. Hirai T, Zelis R, Musch TI. 1995. Effects of nitric oxide synthase inhibition on the muscle blood flow response to exercise in rats with heart failure. Cardiovasc Res 30:469–476.

    PubMed  CAS  Google Scholar 

  26. Armstrong RB, Delp MD, Goljan EF, Laughlin MH. 1987. Distribution of blood flow in muscles of miniature swine during exercise. J Appl Physiol 62:1285–1298.

    PubMed  CAS  Google Scholar 

  27. MacLean MR. 1999. Endothelin-1 and serotonin: mediators of primary and secondary pulmonary hypertension? J Lab Clin Med 134:105–114.

    Article  PubMed  CAS  Google Scholar 

  28. Spinale FG, Grine RC, Tempel GE, Crawford FA, Zile MR. 1992. Alterations in the myocardial capillary vasculature accompany tachycardia-induced cardiomyopathy. Basic Res Cardiol 87:65–79.

    Article  PubMed  CAS  Google Scholar 

  29. Shannon RP, Komamura K, Shen YT, Bishop SP, Vatner SF. 1993. Impaired regional subendocardial coronary flow reserve in conscious dogs with pacing-induced heart failure. Am J Physiol 265:H801–809.

    PubMed  CAS  Google Scholar 

  30. Spinale FG, Hendrick DA, Crawford FA, Smith AC, Hamada Y, Carabello BA. 1990. Chronic supraventricular tachycardia causes ventricular dysfunction and subendocardial injury in swine. Am J Physiol 259:H218–229.

    PubMed  CAS  Google Scholar 

  31. Helmer GA, McKirnan MD, Shabetai R, Boss GR, Ross JJ, Hammond HK. 1996. Regional deficits of myocardial blood flow and function in left ventricular pacing-induced heart failure. Circulation 94:2260–2267.

    Article  PubMed  CAS  Google Scholar 

  32. Bache RJ. 1988. Effects of hypertrophy on the coronary circulation. Prog Cardiovasc Dis 30:403–440.

    Article  PubMed  CAS  Google Scholar 

  33. Vatner SF, Hittinger L. 1993. Myocardial perfusion dependent and independent mechanisms of regional myocardial dysfunction in hypertrophy. Basic Res Cardiol 88:81–95.

    PubMed  Google Scholar 

  34. Treasure CB, Vita JA, Cox DA, Fish RD, Gordon JB, Mudge GH, Colucci WS, Sutton MG, Selwyn AP, Alexander RW, et al. 1990. Endothelium-dependent dilation of the coronary microvasculature is impaired in dilated cardiomyopathy. Circulation 81:772–779.

    Article  PubMed  CAS  Google Scholar 

  35. Katz SD, Biasucci L, Sabba C, Strom JA, Jondeau G, Galvao M, Solomon S, Nikolic SD, Forman R, LeJemtel TH. 1992. Impaired endothelium-mediated vasodilation in the peripheral vasculature of patients with congestive heart failure. J Am Coll Cardiol 19:918–925.

    Article  PubMed  CAS  Google Scholar 

  36. Hambrecht R, Fiehn E, Weigl C, Gielen S, Hamann C, Kaiser R, Yu J, Adams V, Niebauer J, Schuler G. 1998. Regular physical exercise corrects endothelial dysfunction and improves exercise capacity in patients with chronic heart failure. Circulation 98:2709–2715.

    Article  PubMed  CAS  Google Scholar 

  37. Drexler H, Hayoz D, Munzel T, Hornig B, Just H, Brunner HR, Zelis R. 1992. Endothelial function in chronic congestive heart failure. Am J Cardiol 69:1596–1601.

    Article  PubMed  CAS  Google Scholar 

  38. Hirooka Y, Imaizumi T, Tagawa T, Shiramoto M, Endo T, Ando S, Takeshita A. 1994. Effects of L-arginine on impaired acetylcholine-induced and ischemic vasodilation of the forearm in patients with heart failure. Circulation 90:658–668.

    Article  PubMed  CAS  Google Scholar 

  39. Katz SD, Schwarz M, Yuen J, Lejemtel TH. 1993. Impaired acetylcholine-mediated vasodilation in patients with congestive heart failure. Role of endothelium-derived vasodilating and vasoconstricting factors. Circulation 88:55–61.

    Article  PubMed  CAS  Google Scholar 

  40. Maguire SM, Nugent AG, McGurk C, Johnston GD, Nicholls DP. 1998. Abnormal vascular responses in human chronic cardiac failure are both endothelium dependent and endothelium independent. Heart 80:141–145.

    PubMed  CAS  Google Scholar 

  41. Drexler H, Hablawetz E, Lu W, Riede U, Christes A. 1992. Effects of inhibition of nitric oxide formation on regional blood flow in experimental myocardial infarction. Circulation 86:255–262.

    Article  PubMed  CAS  Google Scholar 

  42. Kiuchi K, Sato N, Shannon RP, Vatner DE, Morgan K, Vatner SE 1993. Depressed beta-adrenergic receptor-and endothelium-mediated vasodilation in conscious dogs with heart failure. Circ Res 73:1013–1023.

    Google Scholar 

  43. Kubo SH, Rector TS, Bank AJ, Williams RE, Heifetz SM. 1991. Endothelium-dependent vasodilation is attenuated in patients with heart failure. Circulation 84:1589–1596.

    Article  PubMed  CAS  Google Scholar 

  44. Bank AJ, Lee PC, Kubo SH. 2000. Endothelial dysfunction in patients with heart failure: relationship to disease severity. J Card Fail 6:29–36.

    Article  PubMed  CAS  Google Scholar 

  45. Govers R, Rabelink TJ. 2001. Cellular regulation of endothelial nitric oxide synthase. Am J Physiol Renal Physiol 280:F193–206.

    PubMed  CAS  Google Scholar 

  46. Gaballa MA, Raya TE, Hoover CA, Goldman S. 1999. Effects of endothelial and inducible nitric oxide synthases inhibition on circulatory function in rats after myocardial infarction. Cardiovasc Res 42:627–635.

    Article  PubMed  CAS  Google Scholar 

  47. Ceiler DL, Nelissen-Vrancken M, De Mey JG, Smits JF. 1999. Role of basal nitric oxide synthesis in vasoconstrictor hyporeactivity in the perfused rat hindlimb after myocardial infarction: effect of Captopril. Cardiovasc Res 43:779–787.

    Article  PubMed  CAS  Google Scholar 

  48. Katz SD, Krum H, Khan T, Knecht M. 1996. Exercise-induced vasodilation in forearm circulation of normal subjects and patients with congestive heart failure: role of endothelium-derived nitric oxide. J Am Coll Cardiol 28:585–590.

    Article  PubMed  CAS  Google Scholar 

  49. Kubo SH, Rector TS, Bank AJ, Raij L, Kraemer MD, Tadros P, Beardslee M, Garr MD. 1994. Lack of contribution of nitric oxide to basal vasomotor tone in heart failure. Am J Cardiol 74:1133–1136.

    Article  PubMed  CAS  Google Scholar 

  50. Habib F, Dutka D, Crossman D, Oakley CM, Cleland JG. 1994. Enhanced basal nitric oxide production in heart failure: another failed counter-regulatory vasodilator mechanism? Lancet 344:371–373.

    Article  PubMed  CAS  Google Scholar 

  51. Orus J, Heras M, Morales-Ruiz M, Leivas A, Roig E, Rigol M, Rivera F, Sanz G, Jimenez W. 2000. Nitric oxide synthase II mRNA expression in cardiac tissue of patients with heart failure undergoing cardiac transplantation. J Heart Lung Transplant 19:139–144.

    Article  PubMed  CAS  Google Scholar 

  52. Smith CJ, Sun D, Hoegler C, Roth BS, Zhang X, Zhao G, Xu XB, Kobari Y, Pritchard K, Jr., Sessa WC, Hintze TH. 1996. Reduced gene expression of vascular endothelial NO synthase and cyclooxy-genase-1 in heart failure. Circ Res 78:58–64.

    Article  PubMed  CAS  Google Scholar 

  53. Fukuchi M, Hussain SN, Giaid A. 1998. Heterogeneous expression and activity of endothelial and inducible nitric oxide synthases in end-stage human heart failure: their relation to lesion site and beta-adrenergic receptor therapy. Circulation 98:132–139.

    Article  PubMed  CAS  Google Scholar 

  54. Heymes C, Vanderheyden M, Bronzwaer JG, Shah AM, Paulus WJ. 1999. Endomyocardial nitric oxide synthase and left ventricular preload reserve in dilated cardiomyopathy. Circulation 99:3009–3016.

    Article  PubMed  CAS  Google Scholar 

  55. De Beider AJ, Radomski MW, Why HJ, Richardson PJ, Martin JF. 1995. Myocardial calcium-independent nitric oxide synthase activity is present in dilated cardiomyopathy, myocarditis, and postpartum cardiomyopathy but not in ischaemic or valvar heart disease. Br Heart J 74:426–430.

    Article  Google Scholar 

  56. Stein B, Eschenhagen T, Rudiger J, Scholz H, Forstermann U, Gath I. 1998. Increased expression of constitutive nitric oxide synthase III, but not inducible nitric oxide synthase II, in human heart failure. J Am Coll Cardiol 32:1179–1186.

    Article  PubMed  CAS  Google Scholar 

  57. Haywood GA, Tsao PS, von der Leyen HE, Mann MJ, Keeling PJ, Trindade PT, Lewis NP, Byrne CD, Rickenbacher PR, Bishopric NH, Cooke JP, McKenna WJ, Fowler MB. 1996. Expression of inducible nitric oxide synthase in human heart failure. Circulation 93:1087–1094.

    Article  PubMed  CAS  Google Scholar 

  58. Takimoto Y, Aoyama T, Keyamura R, Shinoda E, Hattori R, Yui Y, Sasayama S. 2000. Differential expression of three types of nitric oxide synthase in both infarcted and non-infarcted left ventricles after myocardial infarction in the rat. Int J Cardiol 76:135–145.

    Article  PubMed  CAS  Google Scholar 

  59. Motte S, Communi D, Pirotton S, Boeynaems JM. 1995. Involvement of multiple receptors in the actions of extracellular ATP: the example of vascular endothelial cells. Int J Biochem Cell Biol 27:1–7.

    Article  PubMed  CAS  Google Scholar 

  60. Dimmeler S, Fleming I, Fisslthaler B, Hermann C, Busse R, Zeiher AM. 1999. Activation of nitric oxide synthase in endothelial cells by Akt-dependent phosphorylation. Nature 399:601–605.

    Article  PubMed  CAS  Google Scholar 

  61. Traverse JH,Wang YL, Du R, Nelson D, Lindstrom P, Archer SL, Gong G, Bache RJ. 2000. Coronary nitric oxide production in response to exercise and endothelium-dependent agonists. Circulation 101:2526–2531.

    Article  PubMed  CAS  Google Scholar 

  62. Radegran G, Saltin B. 1999. Nitric oxide in the regulation of vasomotor tone in human skeletal muscle. Am J Physiol 276:H1951–1960.

    PubMed  CAS  Google Scholar 

  63. Schrier RW, Abraham WT. 1999. Hormones and hemodynamics in heart failure. N Engl J Med 341:577–585.

    Article  PubMed  CAS  Google Scholar 

  64. Moe GW, Stopps TP, Angus C, Forster C, De Bold AJ, Armstrong PW. 1989. Alterations in serum sodium in relation to atrial natriuretic factor and other neuroendocrine variables in experimental pacing-induced heart failure. J Am Coll Cardiol 13:173–179.

    Article  PubMed  CAS  Google Scholar 

  65. Francis GS, Goldsmith SR, Ziesche S, Nakajima H, Cohn JN. 1985. Relative attenuation of sympathetic drive during exercise in patients with congestive heart failure. J Am Coll Cardiol 5:832–839.

    Article  PubMed  CAS  Google Scholar 

  66. Rundqvist B, Elam M, Bergmann-Sverrisdottir Y, Eisenhofer G, Friberg P. 1997. Increased cardiac adrenergic drive precedes generalized sympathetic activation in human heart failure. Circulation 95:169–175.

    Article  PubMed  CAS  Google Scholar 

  67. Albertini M,Vanelli G, Clement MG. 1996. PGI2 and nitric oxide involvement in the regulation of systemic and pulmonary basal vascular tone in the pig. Prostaglandins Leukot Essent Fatty Acids 54:273–278.

    Article  PubMed  CAS  Google Scholar 

  68. Koller A, Sun D, Kaley G. 1993. Role of shear stress and endothelial prostaglandins in flow-and viscosity-induced dilation of arterioles in vitro. Circ Res 72:1276–1284.

    Article  PubMed  CAS  Google Scholar 

  69. Yi GH, Zwas D, Wang J. 2000. Chronic exercise training preserves prostaglandin-induced dilation of epicardial coronary artery during development of heart failure in awake dogs. Prostaglandins Other Lipid Mediat 60:137–151.

    Article  PubMed  CAS  Google Scholar 

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Authors and Affiliations

  1. Experimental Cardiology, Thoraxcenter, The Netherlands

    David B. Haitsma, Daphne Merkus, Daneel Bac, Pieter D. Verdouw & Dirk J. Duncker MD, PhD

  2. Internal Medicine, Erasmus University Rotterdam, Rotterdam, The Netherlands

    Frans Boomsma

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  1. David B. Haitsma
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  2. Daphne Merkus
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  6. Dirk J. Duncker MD, PhD
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Correspondence to Dirk J. Duncker MD, PhD .

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Editors and Affiliations

  1. Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Faculty of Medicine, University of Manitoba, Winnipeg, Canada

    Pawan K. Singal PhD, DSc (Professor), Ian M. C. Dixon PhD (Associate Professor), Lorrie A. Kirshenbaum PhD (Associate Professor) & Naranjan S. Dhalla PhD, MD (HON), DSc (HON) (Distinguished Professor and Director) (Professor),  (Associate Professor),  (Associate Professor) &  (Distinguished Professor and Director)

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Haitsma, D.B., Merkus, D., Bac, D., Boomsma, F., Verdouw, P.D., Duncker, D.J. (2003). Alterations in Hemodynamic and Neurohumoral Responses to Exercise in Swine with Left Ventricular Remodeling Early after Myocardial Infarction: Role of Blunted NO Bioavailability. In: Singal, P.K., Dixon, I.M.C., Kirshenbaum, L.A., Dhalla, N.S. (eds) Cardiac Remodeling and Failure. Progress in Experimental Cardiology, vol 5. Springer, Boston, MA. https://doi.org/10.1007/978-1-4419-9262-8_14

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