Significance of microvascular remodelling for the vascular flow reserve in hypertension

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Standard

Significance of microvascular remodelling for the vascular flow reserve in hypertension. / Jacobsen, Jens Christian Brings; Hornbech, Morten Sonne; von Holstein-Rathlou, Niels-Henrik.

I: Interface Focus, Bind 1, Nr. 1, 06.02.2011, s. 117-31.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Jacobsen, JCB, Hornbech, MS & von Holstein-Rathlou, N-H 2011, 'Significance of microvascular remodelling for the vascular flow reserve in hypertension', Interface Focus, bind 1, nr. 1, s. 117-31. https://doi.org/10.1098/rsfs.2010.0003

APA

Jacobsen, J. C. B., Hornbech, M. S., & von Holstein-Rathlou, N-H. (2011). Significance of microvascular remodelling for the vascular flow reserve in hypertension. Interface Focus, 1(1), 117-31. https://doi.org/10.1098/rsfs.2010.0003

Vancouver

Jacobsen JCB, Hornbech MS, von Holstein-Rathlou N-H. Significance of microvascular remodelling for the vascular flow reserve in hypertension. Interface Focus. 2011 feb. 6;1(1):117-31. https://doi.org/10.1098/rsfs.2010.0003

Author

Jacobsen, Jens Christian Brings ; Hornbech, Morten Sonne ; von Holstein-Rathlou, Niels-Henrik. / Significance of microvascular remodelling for the vascular flow reserve in hypertension. I: Interface Focus. 2011 ; Bind 1, Nr. 1. s. 117-31.

Bibtex

@article{d92007c450b34df38f8aff969e158737,
title = "Significance of microvascular remodelling for the vascular flow reserve in hypertension",
abstract = "Vascular flow reserve (VFR) is the relative increase in tissue perfusion from the resting state to a state with maximum vasodilatation. Longstanding hypertension reduces the VFR, which in turn reduces the maximum working capacity of the tissue. In principle, both inward arteriolar remodelling and rarefaction of the microvascular network may contribute to this reduction. These processes are known to occur simultaneously in the microcirculation of the hypertensive individual and both cause a reduction in the luminal trans-sectional area available for perfusion. Which of them is the main factor responsible for the reduction in VFR is, however, not known. Here we present simulations performed on large microvascular networks to assess the VFR in various situations. Particular attention is paid to the VFR in networks in which the vessels have structurally adapted to a sustained increase in pressure by inward eutrophic remodelling (IER), i.e. by redistributing the same amount of wall material around a smaller lumen. Collectively, the results indicate that the IER may not per se be the main factor responsible for the hypertensive reduction in VFR. Rather, it may be explained by the presence of arteriolar and capillary rarefaction.",
author = "Jacobsen, {Jens Christian Brings} and Hornbech, {Morten Sonne} and {von Holstein-Rathlou}, Niels-Henrik",
year = "2011",
month = feb,
day = "6",
doi = "10.1098/rsfs.2010.0003",
language = "English",
volume = "1",
pages = "117--31",
journal = "Journal of the Royal Society Interface",
issn = "2042-8898",
publisher = "Royal Society, The",
number = "1",

}

RIS

TY - JOUR

T1 - Significance of microvascular remodelling for the vascular flow reserve in hypertension

AU - Jacobsen, Jens Christian Brings

AU - Hornbech, Morten Sonne

AU - von Holstein-Rathlou, Niels-Henrik

PY - 2011/2/6

Y1 - 2011/2/6

N2 - Vascular flow reserve (VFR) is the relative increase in tissue perfusion from the resting state to a state with maximum vasodilatation. Longstanding hypertension reduces the VFR, which in turn reduces the maximum working capacity of the tissue. In principle, both inward arteriolar remodelling and rarefaction of the microvascular network may contribute to this reduction. These processes are known to occur simultaneously in the microcirculation of the hypertensive individual and both cause a reduction in the luminal trans-sectional area available for perfusion. Which of them is the main factor responsible for the reduction in VFR is, however, not known. Here we present simulations performed on large microvascular networks to assess the VFR in various situations. Particular attention is paid to the VFR in networks in which the vessels have structurally adapted to a sustained increase in pressure by inward eutrophic remodelling (IER), i.e. by redistributing the same amount of wall material around a smaller lumen. Collectively, the results indicate that the IER may not per se be the main factor responsible for the hypertensive reduction in VFR. Rather, it may be explained by the presence of arteriolar and capillary rarefaction.

AB - Vascular flow reserve (VFR) is the relative increase in tissue perfusion from the resting state to a state with maximum vasodilatation. Longstanding hypertension reduces the VFR, which in turn reduces the maximum working capacity of the tissue. In principle, both inward arteriolar remodelling and rarefaction of the microvascular network may contribute to this reduction. These processes are known to occur simultaneously in the microcirculation of the hypertensive individual and both cause a reduction in the luminal trans-sectional area available for perfusion. Which of them is the main factor responsible for the reduction in VFR is, however, not known. Here we present simulations performed on large microvascular networks to assess the VFR in various situations. Particular attention is paid to the VFR in networks in which the vessels have structurally adapted to a sustained increase in pressure by inward eutrophic remodelling (IER), i.e. by redistributing the same amount of wall material around a smaller lumen. Collectively, the results indicate that the IER may not per se be the main factor responsible for the hypertensive reduction in VFR. Rather, it may be explained by the presence of arteriolar and capillary rarefaction.

U2 - 10.1098/rsfs.2010.0003

DO - 10.1098/rsfs.2010.0003

M3 - Journal article

C2 - 22419978

VL - 1

SP - 117

EP - 131

JO - Journal of the Royal Society Interface

JF - Journal of the Royal Society Interface

SN - 2042-8898

IS - 1

ER -

ID: 38229066