Control of coronary blood flow during hypoxemia

Research output: Chapter in Book/Report/Conference proceedingConference contribution

23 Citations (Scopus)

Abstract

Coronary vascular resistance is regulated by a variety of factors including arterial pressure, myocardial metabolism, autonomic nervous system as well as arterial O2 tension (hypoxia). Progressive hypoxemia results in graded coronary vasodilation that is significantly more pronounced when arterial O2 tension falls below 40 mmHg. Microvascular studies have demonstrated that O2 has direct effects on vascular smooth muscle likely mediated by O2 sensors located in vessels < 15 μm diameter. Recent data indicates that hypoxia-induced inhibition of the pentose phosphate pathway and the subsequent decreases in NADPH and intracellular Ca2+ represent an important O2 sensing mechanism in vascular smooth muscle. However, in vivo experiments suggest direct microvascular effects of O2 contribute little to hypoxic coronary vasodilation. The vasodilation is mediated, in part, by local vasoactive metabolites produced in proportion to the degree of hypoxemia, reflex-mediated increases in myocardial metabolism and diminished myocardial tissue oxygenation. In particular, production of adenosine has been shown to increase exponentially with the degree of hypoxia and blockade or degradation of adenosine markedly impairs hypoxia-induced coronary vasodilation. Other investigations support the role of endothelial derived relaxing factors (nitric oxide, prostacyclin) in control of coronary blood flow during hypoxia. Additionally, reductions in PO2 hyperpolarize coronary vascular smooth muscle via K+ ATP channels which represent important "end effectors" that significantly contribute to hypoxic coronary vasodilation. Taken together, these data indicate that the coronary vascular response to hypoxia depends on metabolic and endothelial vasodilatory factors that are produced in proportion to the degree of hypoxemia and that function through mechanisms depending on KATP+ channels.

Original languageEnglish
Title of host publicationAdvances in Experimental Medicine and Biology
Pages25-39
Number of pages15
Volume618
DOIs
StatePublished - 2007

Publication series

NameAdvances in Experimental Medicine and Biology
Volume618
ISSN (Print)00652598

Fingerprint

Blood
Vasodilation
Muscle
Metabolism
Adenosine
Vascular Smooth Muscle
Arterial Pressure
Pentoses
KATP Channels
Oxygenation
Neurology
Epoprostenol
End effectors
Metabolites
NADP
Nitric Oxide
Adenosine Triphosphate
Phosphates
Hypoxia
Pentose Phosphate Pathway

Keywords

  • Adenosine
  • Arterial oxygen tension
  • Coronary circulation
  • K channels
  • Nitric oxide

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)

Cite this

Tune, J. (2007). Control of coronary blood flow during hypoxemia. In Advances in Experimental Medicine and Biology (Vol. 618, pp. 25-39). (Advances in Experimental Medicine and Biology; Vol. 618). https://doi.org/10.1007/978-0-387-75434-5-3

Control of coronary blood flow during hypoxemia. / Tune, Johnathan.

Advances in Experimental Medicine and Biology. Vol. 618 2007. p. 25-39 (Advances in Experimental Medicine and Biology; Vol. 618).

Research output: Chapter in Book/Report/Conference proceedingConference contribution

Tune, J 2007, Control of coronary blood flow during hypoxemia. in Advances in Experimental Medicine and Biology. vol. 618, Advances in Experimental Medicine and Biology, vol. 618, pp. 25-39. https://doi.org/10.1007/978-0-387-75434-5-3
Tune J. Control of coronary blood flow during hypoxemia. In Advances in Experimental Medicine and Biology. Vol. 618. 2007. p. 25-39. (Advances in Experimental Medicine and Biology). https://doi.org/10.1007/978-0-387-75434-5-3
Tune, Johnathan. / Control of coronary blood flow during hypoxemia. Advances in Experimental Medicine and Biology. Vol. 618 2007. pp. 25-39 (Advances in Experimental Medicine and Biology).
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