Skip to main content
Log in

Functional characteristics of the coronary microcirculation

Funktionelle Charakterisierung der koronaren Mikrozirkulation

  • Published:
Herz Aims and scope Submit manuscript

Abstract

For over 50 years, it has been recognized that coronary blood flow is precisely matched to cardiac metabolism. The interactions which govern this matching remain unknown. In the current review, 3 specific aspects of coronary flow regulation will be discussed: Specialization of function in different microvascular domains, influence of cardiac region on microvascular function and the interactions of vasoactive agents in control of coronary blood flow.

Each level of the coronary microcirculation is affected by different physical and chemical forces within the heart. These forces place special demands on these vessels and are in turn met by specialized vasodilator responses, including metabolic and flow-mediated vasodilation. Perfusion of the heart is also profoundly affected by the region perfused. The endocardium is affected by forces, notably cardiac contraction, in a different manner than the epicardium. Thus, the microcirculation has specialized to meet these demands. Finally, the factors determining microvascular tone appear to be coordinated such that the loss of any individual dilator, such as nitric oxide, can be compensated for by the increased contribution of another, such as adenosine. This interplay may serve to protect the heart from ischemia during the early phases of coronary vascular disease when individual dilators may be impaired.

Zusammenfassung

Seit über 50 Jahren ist die Beziehung zwischen koronarer Durchblutung und Myokardmetabolismus bekannt. Die Interaktion zwischen den einzelnen Kontrollsystemen zur Regulation der Koronardurchblutung, die funktionelle Bedeutung der mikrovaskulären Strombahn und der Anfluß der Myokardregion auf die mikrovaskuläre Funktion sind jedoch weitgehend ungeklärt. Drei wesentliche Mechanismen existieren, die den Koronartonus regulieren: 1. die metabolische Regulation, 2. die flußabhängige Regulation, 3. die Autoregulation. Die physiologische Anpassung des mikrovaskulären Tonus ist eng verbunden mit dem kardialen Sauerstoffverbrauch. Eine Steigerung des myokardialen Sauerstoff-verbrauchs führt zu einer Dilatation der mikrovaskulären Gefäße. Dies ist bekannt als metabolische Dilatation oder funktionelle Hyperämie. Die schnelle Stimulation steigert den myokardialen Sauerstoffverbrauch. Die Reaktion der mikrovaskulären Gefäße ist heterogen. Die kleinen Arteriolen sind besonders verantwortlich für die koronare Flußsteigerung während der metabolischen Dilatation. Adenosin induziert eine Dilatation der kleinen und größeren Arteriolen. Die Regulation der epikardialen Koronarterienweite ist bekannt. Die Dilatation geht verloren, wenn akut oder chronisch NO blockiert wird, während der Anstieg der Koronardurchblutung als Reaktion auf metabolische Effekte oder pharmakologische Eingriffe erhalten ist. Neuere Untersuchungen weisen darauf hin, daß die flußabhängige Dilatation nicht nur die epikardialen Gefäße, sondern auch die koronare Mikrozirkulation erreicht. Die Autoregulation ist definiert als die intrinsische Eigenschaft, den Koronarfluß bei Änderungen des koronaren Perfusionsdruckes unabhängig von Änderungen des Metabolismus aufrechtzuerhalten. Als Antwort auf physiologische Eingriffe reagiert das koronare mikrovaskuläre Gebiet heterogen und nicht einheitlich. Das atriale mikrovaskuläre System ist geringer ausgeprägt als das ventrikuläre System. Die Dilatation nach Gabe von Adenosin, Bradykinin und Substanz P ist ähnlich. Als Folge findet sich eine einigermaßen gleichmäßige Perfusion aller Myokardregionen. Die großen Unterschiede in bezug auf den Koronarfluß, die in verschiedenen Regionen bei reduziertem Perfusionsdruck beobachtet werden, sind hauptsächlich abhängig von physikalischen Faktoren, wie die Kontraktion des Myokards.

NO spielt eine zentrale Rolle in der Regulation des koronaren vaskulären Tonus. Wichtig ist, daß verschiedene potentielle Dilatatoren zur Verfügung stehen, wenn selbst NO gehemmt wird.

Multiple Mediatoren formen ein interaktives Netzwerk, das das Herz vor den Schädigungen, induziert durch Ischämie, schützt und die Anpassung an Belastungen ermöglicht. Diese Mediatoren spielen wahrscheinlich eine wichtige Rolle in der Frühphase der koronaren Herzerkrankung.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others

References

  1. Altman JD, Kinn J, Duncker DJ, et al. Effect of inhibition of nitric oxide formation on coronary blood flow during exercise in the dog. Cardiovasc Res 1994;28:119–24.

    Article  PubMed  CAS  Google Scholar 

  2. Ando J, Kamiya A. Flow-dependent regulation of gene expression in vascular endothelial cells. [Review] [40 refs]. Jpn Heart J 1996;37:19–32.

    PubMed  CAS  Google Scholar 

  3. Ashikawa K, Kanatsuka H, Suzuki T, et al. Phasic blood flow velocity pattern in epimyocardial microvessels in the beating canine left ventricle. Circ Res 1986;59:704–11.

    PubMed  CAS  Google Scholar 

  4. Austin RE Jr, Aldea GS, Coggins DL, et al. Profound spatial heterogeneity of coronary reserve. Discordance between patterns of resting and maximal myocardial blood flow. Circ Res 1990;67:319–31.

    PubMed  Google Scholar 

  5. Ayajiki K, Kindermann M, Hecker M, et al. Intracellular pH and tyrosine phosphorylation but not calcium determine shear stress-induced nitric oxide production in native endothelial cells [see comments]. Circ Res 1996;78:750–8.

    PubMed  CAS  Google Scholar 

  6. Bauersachs J, Popp R, Hecker M, et al. Nitric oxide attenuates the release of endothelium-derived hyperpolarizing factor. Circulation 1996;94:3341–7.

    PubMed  CAS  Google Scholar 

  7. Belloni FL., Hintze TH. Glibenclamide attenuates adenosine-induced bradycardia and coronary vasodilatation. Am J Physiol 1990;261:H720–7.

    Google Scholar 

  8. Berne RM. Cardiac nucleotides in hypoxia: possible role in regulation of coronary blood flow. Am J Physiol 1963;204:317–22.

    PubMed  CAS  Google Scholar 

  9. Campbell WB, Gebremedhin D, Pratt PF, et al. Identification of epoxyeicosatrienoic acids as endothelium-derived hyperpolarizing factors. Circ Res 1996;78:415–23.

    PubMed  CAS  Google Scholar 

  10. Canty JM Jr, Schwartz JS. Nitric oxide mediates flow-dependent epicardial coronary vasodilation to changes in pulse frequency but not mean flow in conscious dogs. Circulation 1994;89:375–84.

    PubMed  CAS  Google Scholar 

  11. Capdevila J, Gil L, Orellana M, et al. Inhibitors of cytochrome P-450-dependent arachidonic acid metabolism. Arch Biochem Biophys 1988;261:257–63.

    Article  PubMed  CAS  Google Scholar 

  12. Chilian WM. Microvascular pressures and resistances in the left ventricular subepicardium and subendocardium. Circ Res 1991; 69:561–70.

    PubMed  CAS  Google Scholar 

  13. Chilian WM. Functional distribution of α1- and α2-adrenergic receptors in the coronary microcirculation. Circulation 1991;84:2108–22.

    PubMed  CAS  Google Scholar 

  14. Chilian WM, Eastham CL, Marcus ML. Microvascular distribution of coronary vascular resistance in beating left ventricle. Am J Physiol 1986;251:H779–88.

    PubMed  CAS  Google Scholar 

  15. Chilian WM, Layne SM. Coronary microvascular responses to reductions in perfusion pressure: Evidence for persistent arteriolar vasomotor tone during coronary hypoperfusion. Circ Res 1990;66:1227–38.

    PubMed  CAS  Google Scholar 

  16. Chilian WM, Layne SM, Eastham CL, et al. Heterogeneous microvascular coronary α-adrenergic vasoconstriction. Circ Res 1989;64:376–88.

    PubMed  CAS  Google Scholar 

  17. Coggins DL, Flynn AE, Austin RE Jr, et al. Nonuniform loss of regional flow reserve during myocardial ischemia in dogs. Circ Res 1990;67:253–64.

    PubMed  CAS  Google Scholar 

  18. Corriu C, Feletou M, Puybasset L, et al. Endothelium-dependent hyperpolarization in isolated arteries taken from animals treated with NO-synthase inhibitors. J Cardiovasc Pharmacol 1998;32:944–50.

    Article  PubMed  CAS  Google Scholar 

  19. Dankelman J, van der Ploeg CPB, Spaan JAE. Glibenclamide decelerates the responses of coronary regulation in the goat. Am J Physiol 1994;266:H1715–21.

    PubMed  CAS  Google Scholar 

  20. Daut J, Maier-Rudolph W, von Beckerath N, et al. Hypoxic dilation of coronary arteries is mediated by ATP-sensitive potassium channels. Science 1990;247:1341–4.

    Article  PubMed  CAS  Google Scholar 

  21. Davies PF. Endothelium as a signal transduction interface for flow forces: cell surface dynamics. Thromb Haemost 1993;70:1–5.

    Google Scholar 

  22. Dellsperger KC. Potassium channels and the coronary circulation. Clin Exp Pharmacol Physiol 1996;23:1096–101.

    Article  PubMed  CAS  Google Scholar 

  23. Dole WP, Yamada N, Bishop VS, et al. Role of adenosine in coronary blood flow regulation after reductions in perfusion pressure. Circ Res 1985;56:517–24.

    PubMed  CAS  Google Scholar 

  24. Duncker DJ, van Zon NS, Ishibashi Y, et al. Role of K+ ATP channels and adenosine in the regulation of coronary blood flow during exercise with normal and restricted coronary blood flow. J Clin Invest 1996;97:996–1009.

    Article  PubMed  CAS  Google Scholar 

  25. Duran WN. Regulation of coronary microvascular perfusion: roles of adenosine and PO2 in capillary recruitment. In: Merrill GF, Weiss HR, eds. Ca2+ entry blockers, adenosine, and neurohumors. Baltimore: Urban & Schwarzenberg, 1983:207–21.

    Google Scholar 

  26. Eckenhoff JE, Hafkenschiel JH, Landmesser CM, et al. Cardiac oxygen metabolism and the control of the coronary circulation. Am J Physiol 1947;149:634–9.

    CAS  Google Scholar 

  27. Egashira K, Katsuda Y, Mohri M, et al. Role of endothelium-derived nitric oxide in coronary vasodilatation induced by pacing tachycardia in humans. Circ Res 1996;79:331–5.

    PubMed  CAS  Google Scholar 

  28. Embrey RP, Brooks LA, Dellsperger KC. Mechanism of coronary microvascular response to metabolic stimulation. Cardiovasc Res 1997;35:148–57.

    Article  PubMed  CAS  Google Scholar 

  29. Feigl EO. Coronary physiology. Physiol Rev 1983;63:1–206.

    PubMed  CAS  Google Scholar 

  30. Feletou M, Vanhoutte PM. Endothelium-dependent hyperpolarization of canine coronary smooth muscle. Br J Pharmacol 1988;93:515–24.

    PubMed  CAS  Google Scholar 

  31. Fleming I, Bauersachs J, Fisslthaler B, et al. Ca2+-independent activation of the endothelial nitric oxide synthase in response to tyrosine phosphatase inhibitors and fluid shear stress. Circ Res 1998;82:686–95.

    PubMed  CAS  Google Scholar 

  32. Fujii M, Nuno DW, Lamping KG, et al. Effect of hypertension and hypertrophy on coronary microvascular pressure. Circ Res 1992;71:120–6.

    PubMed  CAS  Google Scholar 

  33. Gattullo D, Linden RJ, Merletti A, et al. Endothelium and coronary reactive hyperaemia. Boll Soc Ital Speriment 1993;69:431–7.

    CAS  Google Scholar 

  34. Gattullo D, Pagliaro P, Linden RJ, et al. The role of nitric oxide in the initiation and in the duration of some vasodilator responses in the coronary circulation. Pfluegers Arch — Eur J Physiol 1995;430:96–104.

    Article  CAS  Google Scholar 

  35. Godecke A, Decking UKM, Ding Z, et al. Coronary hemodynamics in endothelial NO synthase knockout mice. Circ Res 1998;82:186–94.

    PubMed  CAS  Google Scholar 

  36. Hanley FL, Grattan MT, Stevens MB, et al. Role of adenosine in coronary autoregulation. Am J Physiol 1986;250:H558–66.

    PubMed  CAS  Google Scholar 

  37. Heras M, Roig E, Perez-Villa F, et al. The role of endogenous nitric oxide in the response of coronary blood flow to tachycardia. Cor Art Dis 1996;7:149–54.

    Article  CAS  Google Scholar 

  38. Hintze TH, Vatner SF. Reactive dilation of large coronary arteries in conscious dogs. Circ Res 1984;54:50–7.

    PubMed  CAS  Google Scholar 

  39. Hoffman JIE. Transmural myocardial perfusion. Prog Cardiovasc Dis 1987;29:429–64.

    Article  PubMed  CAS  Google Scholar 

  40. Hoffman JIE. Coronary flow reserve. Curr Opin Cardiol 1988;3:874–80.

    Article  Google Scholar 

  41. Huckstorf C, Zanzinger J, Fink B, et al. Reduced nitric oxide formation causes coronary vasoconstriction and impaired dilator responses to endogenous agonists and hypoxia in dogs. Naunyn Schmiedebergs Arch Pharmacol 1994;349:367–73.

    Article  PubMed  CAS  Google Scholar 

  42. Ishibashi Y, Duncker DJ, Zhang J, et al. ATP-sensitive K+ channels, adenosine, and nitric oxide-mediated mechanisms account for coronary vasodilation during exercise. Circ Res 1998;82:346–59.

    PubMed  CAS  Google Scholar 

  43. Jones CJH, Kuo L, Davis MJ, et al. Role of nitric oxide in the coronary microvascular responses to adenosine and increased metabolic demand. Circulation 1995;91:1807–13.

    PubMed  CAS  Google Scholar 

  44. Kajiya F. Temporal and spatial heterogeneity of blood supply to the heart: visualization and interpretation. Meth Inform Med 1997;36:319–21.

    PubMed  CAS  Google Scholar 

  45. Kajiya F, Ogasawara Y, Hiramatsu O, et al. The relationship between cardiac contraction and intramyocardial hemodynamics. IEEE Engin Med Biol Magazine 1997;16:127–32.

    Article  CAS  Google Scholar 

  46. Kanatsuka H, Lamping KG, Eastham CL, et al. Comparison of the effects of increased myocardial oxygen comsumption and adenosine on the coronary microvascular resistance. Circ Res 1989;65:1296–305.

    PubMed  CAS  Google Scholar 

  47. Kanatsuka H, Lamping KG, Eastham CL, et al. Heterogeneous changes in epimyocardial microvascular size during graded coronary stenosis. Evidence of the microvascular site of autoregulation. Circ Res 1990;66:389–96.

    PubMed  CAS  Google Scholar 

  48. Kanatsuka H, Sekiguchi N, Sato K, et al. Microvascular sites and mechanisms responsible for reactive hyperemia in the coronary circulation of the beating canine heart. Circ Res 1992;71:912–22.

    PubMed  CAS  Google Scholar 

  49. Katsuda Y, Egashira K, Akatsuka Y, et al. Endothelium-derived nitric oxide does not modulate metabolic coronary vasodilation induced by tachycardia in dogs. J Cardiovasc Pharmacol 1995;26:437–44.

    Article  PubMed  CAS  Google Scholar 

  50. Kimura A, Hiramatsu O, Wada Y, et al. Atrial contractility affects phasic blood flow velocity of atrial small vessels in the dog. Cardiovasc Res 1992;26:1219–25.

    Article  PubMed  CAS  Google Scholar 

  51. Koller A, Kaley G. Endothelial regulation of wall shear stress and blood flow in skeletal muscle microcirculation. Am J Physiol 1991;260:H862–8.

    PubMed  CAS  Google Scholar 

  52. Komaru T, Lamping KG, Eastham CL, et al. Role of ATP-sensitive potassium channels in coronary microvascular autoregulatory responses. Circ Res 1991;69:1146–51.

    PubMed  CAS  Google Scholar 

  53. Kostic MM, Schrader J. Role of nitric oxide in reactive hyperemia of the guinea pig heart. Circ Res 1992;70:208–12.

    PubMed  CAS  Google Scholar 

  54. Kuo L, Davis MJ, Chilian WM. Myogenic activity in isolated subepicardial and subendocardial coronary arterioles. Am J Physiol 1988;255:H1558–62.

    PubMed  CAS  Google Scholar 

  55. Kuo L, Davis MJ, Chilian WM. Endothelium-dependent, flow-induced dilation of isolated coronary arterioles. Am J Physiol 1990;259:H1063–70.

    PubMed  CAS  Google Scholar 

  56. Kuo L, Davis MJ, Chilian WM. Interaction of pressure-and flow-induced responses in porcine resistance vessels. Am J Physiol 1991;261:H1706–15.

    PubMed  CAS  Google Scholar 

  57. Kuo L, Davis MJ, Chilian WM. Longitudinal gradients for endothelium-dependent and-independent vascular responses in the coronary circulation. Circulation 1995;92:518–25.

    PubMed  CAS  Google Scholar 

  58. Lamontagne D, Pohl U, Busse R. Mechanical deformation of vessel wall and shear stress determine the basal release of endothelium-derived relaxing factor in the intact rabbit coronary vascular bed. Circ Res 1992;70:123–30.

    PubMed  CAS  Google Scholar 

  59. Lamping KG, Kanatsuka H, Eastham CL, et al. Nonuniform vasomotor responses of the coronary microcirculation to serotonin and vasopressin. Circ Res 1989;65:343–51.

    PubMed  CAS  Google Scholar 

  60. Maekawa K, Saito D, Obayashi N, et al. Role of endothelium-derived nitric oxide and adenosine in functional myocardial hyperemia. Am J Physiol 1994;267:H166–73.

    PubMed  CAS  Google Scholar 

  61. Malek AM, Izumo S. Control of endothelial cell gene expression by flow. J Biomech 1995;28:1515–28.

    Article  PubMed  CAS  Google Scholar 

  62. May-Newman K, Mathieu-Costello O, Omens JH, et al. Transmural distribution of capillary morphology as a function of coronary perfusion pressure in the resting canine heart. Microvasc Res 1995;50:381–96.

    Article  PubMed  CAS  Google Scholar 

  63. Merkus D, Kajiya F, Vink H, et al. Prolonged diastolic time fraction protects myocardial perfusion when coronary blood flow is reduced. Circulation (in press).

  64. Miller FJ, Dellsperger KC, Embrey RP, et al. Isolated human coronary arterioles exhibit myogenic tone. Circulation 1993;88:980. abstract.

    Google Scholar 

  65. Miller FJ Jr, Dellsperger KC, Gutterman DD. Myogenic constriction of human coronary arterioles. Am J Physiol 1997;273:H257–64.

    PubMed  CAS  Google Scholar 

  66. Miller FJ Jr, Dellsperger KC, Gutterman DD. Pharmacologic activation of the human coronary microcirculation in vitro: endothelium-dependent dilation and differential responses to acetylcholine. Cardiol Res 1998;38:744–50.

    Article  CAS  Google Scholar 

  67. Minamino T, Kitakaze M, Node K, et al. Inhibition of nitric oxide synthesis increases adenosine production via an extracellular pathway through activation of protein kinase C. Circulation 1997;96:1586–92.

    PubMed  CAS  Google Scholar 

  68. Miura H, Gutterman DD. Human coronary arteriolar dilation to arachidonic acid depends on cytochrome P-450 monooxygenase and Ca2+-activated K+ channels. Circ Res 1998;83:501–7.

    PubMed  CAS  Google Scholar 

  69. Muller JM, Chilian WM, Davis MJ. Integrin signaling tranduces shear stress-dependent vasodilation of coronary arterioles. Circ Res 1997;80:320–6.

    PubMed  CAS  Google Scholar 

  70. Muller JM, Davis MJ, Chilian WM. Coronary arteriolar flow-induced vasodilation signals through tyrosine kinase. Am J Physiol 1996;270:H1878–84.

    PubMed  CAS  Google Scholar 

  71. Nuller JM, Davis MJ, Kuo L, et al. Changes in coronary endothelial cell Ca2+ concentration during shear stress- and agonist-induced vasodilation. Am J Physiol 1999;276:H1706–14.

    Google Scholar 

  72. Narishige T, Egashira K, Akatsuka Y, et al. Glibenciamide, a putative ATP-sensitive K+ channel blocker, inhibits coronary autoregulation in anesthetized dogs. Circ Res 1993;73:771–6.

    PubMed  CAS  Google Scholar 

  73. Nishikawa Y, Ogawa S. Importance of nitric oxide in the coronary artery at rest and during pacing in humans. J Am Coll Cardiol 1997;29:85–92.

    Article  PubMed  CAS  Google Scholar 

  74. Nishikawa Y, Stepp DW, Chilian WM. Role of endothelium-dependent hyperpolarizing factor in the canine coronary microcirculation. Am J Physiol (in press).

  75. Oltman CL, Weintraub NL, VanRollins M, et al. Epoxyeicosatrienoic acids and dihydroxyeicosatrienoic acids are potent vasodilators in the canine coronary microcirculation. Circ Res 1998;83:932–9.

    PubMed  CAS  Google Scholar 

  76. Ortiz de Montellano PR, Mico BA, Mathews JM, et al. Selective inactivation of cytochrome P-450 isozymes by suicide substrates. Arch Biochem Biophys 1981;210:717–28.

    Article  PubMed  CAS  Google Scholar 

  77. Puybasset L, Bea M, Ghaleh B, et al. Coronary and systemic hemodynamic effects of sustained inhibition of nitric oxide synthesis and cyclooxygenase in coronary vessels. Circ Res 1996; 79:343–57.

    PubMed  CAS  Google Scholar 

  78. Puybasset L, Beverelli F, Giudicelli JF, et al. Prostaglandins reduce the contractile responses to noradrenaline and angiotensin II in canine femoral arteries after but not before chornic inhibition of nitric oxide synthesis. J Cardiovasc Pharmacol 1997; 30:690–4.

    Article  PubMed  CAS  Google Scholar 

  79. Quillen JE, Harrison DG. Vasomotor properties of porcine endocardial and epicardial microvessels. Am J Physiol 1992;262:H1143–8.

    PubMed  CAS  Google Scholar 

  80. Ouyyumi AA, Dakak N, Andrews NP, et al. Contribution of nitric oxide to metabolic coronary vasodilation in the human heart. Circulation 1995;92:320–6.

    Google Scholar 

  81. Rembert JC, Boyd LM, Watkinson WP, et al. Effect of adenosine on transmural myocardial blood flow distribution in the awake dog. Am J Physiol 1980;239:H7–13.

    PubMed  CAS  Google Scholar 

  82. Shiode N, Morishima N, Nakayama K, et al. Flow-mediated vasodilation of human epicardial arteries: effect of inhibition of nitric oxide synthesis. J Am Coll Cardiol 1998;27:304–10.

    Article  Google Scholar 

  83. Solzbach U, Liao J, Eigler NL, et al. Effects of inhibition of nitric oxide formation on the regulation of coronary blood flow in anesthetized dogs. Basic Res Cardiol 1998;90:489–97.

    Article  Google Scholar 

  84. Stepp DW, Kroll K, Feigl EO. K+ATP channels and adenosine are not necessary for coronary autoregulation. Am J Physiol 1997;273:H1299–308.

    PubMed  CAS  Google Scholar 

  85. Stepp DW, Nishikawa Y, Chilian WM. Regulation of shear stress in the coronary microcirculation. Circulation (in press).

  86. Stepp DW, van Bibber R, Kroll K, et al. Quantitative relation between interstitial adenosine concentration and coronary blood flow. Circ Res 1996;79:601–10.

    PubMed  CAS  Google Scholar 

  87. Tanaka E, Mori H, Chujo M, et al. Coronary vasoconstrictive effects of neuropeptide Y and their modulation by the ATP-sensitive potassium channel in anesthetized dogs. J Am Coll Cardiol 1997;29:1380–89.

    Article  PubMed  CAS  Google Scholar 

  88. Tayama S, Okumura K, Matsunaga T, et al. Influence of chronic nitric oxide inhibition on coronary blood flow regulation: A study of the role of endogenous adenosine in anesthetized open-chest dogs. Jpn Circ J 1998;62:371–8.

    Article  PubMed  CAS  Google Scholar 

  89. Tomanek RJ, Palmer PJ, Peiffer GL, et al. Morphometry of canine coronary arteries, arterioles, and capillaries during hypertension and left ventricular hypertrophy. Circ Res 1986;58:38–46.

    PubMed  CAS  Google Scholar 

  90. Wei HM, Kang YH, Merril GF. Canine coronary vasodepressor responses to hypoxia are abolished by 8-phenyltheophylline. Am J Physiol 1978;257:H1043–8.

    Google Scholar 

  91. Weiss HR, Conway RS. Morphometric study of the total and perfused arteriolar and capillary network of the rabbit left ventricle. Cardiovasc Res 1985;19:343–54.

    Article  PubMed  CAS  Google Scholar 

  92. Widmann MD, Weintraub NL, Fudge JL, et al. Cytochrome P-450 pathway in acetylcholine-induced canine coronary microvascular vasodilation in vivo. Am J Physiol 1998;274:H283–9.

    PubMed  CAS  Google Scholar 

  93. Wusten B, Buss DD, Diest H, et al. Dilatory capacity of the coronary circulation and its correlation to the arterial vasculature in the canine left ventricle. Basic Res Cardiol 1977;72:636–50.

    Article  PubMed  CAS  Google Scholar 

  94. Yada T, Hiramatsu O, Kimura A, et al. In vivo observation of subendocardial microvessels of the beating porcine heart using a needle-probe video-microscope with a CCD camera. Circ Res 1993;60:100–200.

    Google Scholar 

  95. Yada T, Hiramatsu O, Kimura A, et al. Direct in vivo observation of subendocardial arteriolar response during reactive hyperemia. Circ Res 1995;77:622–31.

    PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to David W. Stepp Ph. D..

Rights and permissions

Reprints and permissions

About this article

Cite this article

Merkus, D., Chilian, W.M. & Stepp, D.W. Functional characteristics of the coronary microcirculation. Herz 24, 496–508 (1999). https://doi.org/10.1007/BF03044220

Download citation

  • Issue Date:

  • DOI: https://doi.org/10.1007/BF03044220

Key Words

Schlüsselwörter

Navigation