The role of the cerebral capillaries in acute ischemic stroke: the extended penumbra model.

Standard

The role of the cerebral capillaries in acute ischemic stroke: the extended penumbra model. / Østergaard, Leif; Jespersen, Sune Nørhøj; Mouridsen, Kim; Mikkelsen, Irene Klærke; Jonsdottír, Kristjana Ýr; Tietze, Anna; Blicher, Jakob Udby; Aamand, Rasmus; Hjort, Niels; Iversen, Nina Kerting; Cai, Changsi; Hougaard, Kristina Dupont; Simonsen, Claus Z; Paul, Von Weitzel-Mudersbach; Modrau, Boris; Nagenthiraja, Kartheeban; Lars, Riisgaard Ribe; Hansen, Mikkel Bo; Bekke, Susanne Lise; Dahlman, Martin Gervais; Puig, Josep; Pedraza, Salvador; Serena, Joaquín; Cho, Tae-Hee; Siemonsen, Susanne; Thomalla, Götz; Fiehler, Jens; Nighoghossian, Norbert; Andersen, Grethe.

in: J CEREBR BLOOD F MET, Jahrgang 33, Nr. 5, 5, 2013, S. 635-648.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Østergaard, L, Jespersen, SN, Mouridsen, K, Mikkelsen, IK, Jonsdottír, KÝ, Tietze, A, Blicher, JU, Aamand, R, Hjort, N, Iversen, NK, Cai, C, Hougaard, KD, Simonsen, CZ, Paul, VW-M, Modrau, B, Nagenthiraja, K, Lars, RR, Hansen, MB, Bekke, SL, Dahlman, MG, Puig, J, Pedraza, S, Serena, J, Cho, T-H, Siemonsen, S, Thomalla, G, Fiehler, J, Nighoghossian, N & Andersen, G 2013, 'The role of the cerebral capillaries in acute ischemic stroke: the extended penumbra model.', J CEREBR BLOOD F MET, Jg. 33, Nr. 5, 5, S. 635-648. <http://www.ncbi.nlm.nih.gov/pubmed/23443173?dopt=Citation>

APA

Østergaard, L., Jespersen, S. N., Mouridsen, K., Mikkelsen, I. K., Jonsdottír, K. Ý., Tietze, A., Blicher, J. U., Aamand, R., Hjort, N., Iversen, N. K., Cai, C., Hougaard, K. D., Simonsen, C. Z., Paul, V. W-M., Modrau, B., Nagenthiraja, K., Lars, R. R., Hansen, M. B., Bekke, S. L., ... Andersen, G. (2013). The role of the cerebral capillaries in acute ischemic stroke: the extended penumbra model. J CEREBR BLOOD F MET, 33(5), 635-648. [5]. http://www.ncbi.nlm.nih.gov/pubmed/23443173?dopt=Citation

Vancouver

Østergaard L, Jespersen SN, Mouridsen K, Mikkelsen IK, Jonsdottír KÝ, Tietze A et al. The role of the cerebral capillaries in acute ischemic stroke: the extended penumbra model. J CEREBR BLOOD F MET. 2013;33(5):635-648. 5.

Bibtex

@article{07ac3830fa174618bda787c144df0ff6,
title = "The role of the cerebral capillaries in acute ischemic stroke: the extended penumbra model.",
abstract = "The pathophysiology of cerebral ischemia is traditionally understood in relation to reductions in cerebral blood flow (CBF). However, a recent reanalysis of the flow-diffusion equation shows that increased capillary transit time heterogeneity (CTTH) can reduce the oxygen extraction efficacy in brain tissue for a given CBF. Changes in capillary morphology are typical of conditions predisposing to stroke and of experimental ischemia. Changes in capillary flow patterns have been observed by direct microscopy in animal models of ischemia and by indirect methods in humans stroke, but their metabolic significance remain unclear. We modeled the effects of progressive increases in CTTH on the way in which brain tissue can secure sufficient oxygen to meet its metabolic needs. Our analysis predicts that as CTTH increases, CBF responses to functional activation and to vasodilators must be suppressed to maintain sufficient tissue oxygenation. Reductions in CBF, increases in CTTH, and combinations thereof can seemingly trigger a critical lack of oxygen in brain tissue, and the restoration of capillary perfusion patterns therefore appears to be crucial for the restoration of the tissue oxygenation after ischemic episodes. In this review, we discuss the possible implications of these findings for the prevention, diagnosis, and treatment of acute stroke.",
keywords = "Animals, Humans, Models, Biological, Oxygen/metabolism, Brain/*blood supply/metabolism/*physiopathology, Brain Ischemia/diagnosis/metabolism/*physiopathology/prevention & control, Capillaries/metabolism/*physiopathology, *Cerebrovascular Circulation, Stroke/diagnosis/metabolism/*physiopathology/prevention & control, Animals, Humans, Models, Biological, Oxygen/metabolism, Brain/*blood supply/metabolism/*physiopathology, Brain Ischemia/diagnosis/metabolism/*physiopathology/prevention & control, Capillaries/metabolism/*physiopathology, *Cerebrovascular Circulation, Stroke/diagnosis/metabolism/*physiopathology/prevention & control",
author = "Leif {\O}stergaard and Jespersen, {Sune N{\o}rh{\o}j} and Kim Mouridsen and Mikkelsen, {Irene Kl{\ae}rke} and Jonsdott{\'i}r, {Kristjana {\'Y}r} and Anna Tietze and Blicher, {Jakob Udby} and Rasmus Aamand and Niels Hjort and Iversen, {Nina Kerting} and Changsi Cai and Hougaard, {Kristina Dupont} and Simonsen, {Claus Z} and Paul, {Von Weitzel-Mudersbach} and Boris Modrau and Kartheeban Nagenthiraja and Lars, {Riisgaard Ribe} and Hansen, {Mikkel Bo} and Bekke, {Susanne Lise} and Dahlman, {Martin Gervais} and Josep Puig and Salvador Pedraza and Joaqu{\'i}n Serena and Tae-Hee Cho and Susanne Siemonsen and G{\"o}tz Thomalla and Jens Fiehler and Norbert Nighoghossian and Grethe Andersen",
year = "2013",
language = "English",
volume = "33",
pages = "635--648",
journal = "J CEREBR BLOOD F MET",
issn = "0271-678X",
publisher = "SAGE Publications",
number = "5",

}

RIS

TY - JOUR

T1 - The role of the cerebral capillaries in acute ischemic stroke: the extended penumbra model.

AU - Østergaard, Leif

AU - Jespersen, Sune Nørhøj

AU - Mouridsen, Kim

AU - Mikkelsen, Irene Klærke

AU - Jonsdottír, Kristjana Ýr

AU - Tietze, Anna

AU - Blicher, Jakob Udby

AU - Aamand, Rasmus

AU - Hjort, Niels

AU - Iversen, Nina Kerting

AU - Cai, Changsi

AU - Hougaard, Kristina Dupont

AU - Simonsen, Claus Z

AU - Paul, Von Weitzel-Mudersbach

AU - Modrau, Boris

AU - Nagenthiraja, Kartheeban

AU - Lars, Riisgaard Ribe

AU - Hansen, Mikkel Bo

AU - Bekke, Susanne Lise

AU - Dahlman, Martin Gervais

AU - Puig, Josep

AU - Pedraza, Salvador

AU - Serena, Joaquín

AU - Cho, Tae-Hee

AU - Siemonsen, Susanne

AU - Thomalla, Götz

AU - Fiehler, Jens

AU - Nighoghossian, Norbert

AU - Andersen, Grethe

PY - 2013

Y1 - 2013

N2 - The pathophysiology of cerebral ischemia is traditionally understood in relation to reductions in cerebral blood flow (CBF). However, a recent reanalysis of the flow-diffusion equation shows that increased capillary transit time heterogeneity (CTTH) can reduce the oxygen extraction efficacy in brain tissue for a given CBF. Changes in capillary morphology are typical of conditions predisposing to stroke and of experimental ischemia. Changes in capillary flow patterns have been observed by direct microscopy in animal models of ischemia and by indirect methods in humans stroke, but their metabolic significance remain unclear. We modeled the effects of progressive increases in CTTH on the way in which brain tissue can secure sufficient oxygen to meet its metabolic needs. Our analysis predicts that as CTTH increases, CBF responses to functional activation and to vasodilators must be suppressed to maintain sufficient tissue oxygenation. Reductions in CBF, increases in CTTH, and combinations thereof can seemingly trigger a critical lack of oxygen in brain tissue, and the restoration of capillary perfusion patterns therefore appears to be crucial for the restoration of the tissue oxygenation after ischemic episodes. In this review, we discuss the possible implications of these findings for the prevention, diagnosis, and treatment of acute stroke.

AB - The pathophysiology of cerebral ischemia is traditionally understood in relation to reductions in cerebral blood flow (CBF). However, a recent reanalysis of the flow-diffusion equation shows that increased capillary transit time heterogeneity (CTTH) can reduce the oxygen extraction efficacy in brain tissue for a given CBF. Changes in capillary morphology are typical of conditions predisposing to stroke and of experimental ischemia. Changes in capillary flow patterns have been observed by direct microscopy in animal models of ischemia and by indirect methods in humans stroke, but their metabolic significance remain unclear. We modeled the effects of progressive increases in CTTH on the way in which brain tissue can secure sufficient oxygen to meet its metabolic needs. Our analysis predicts that as CTTH increases, CBF responses to functional activation and to vasodilators must be suppressed to maintain sufficient tissue oxygenation. Reductions in CBF, increases in CTTH, and combinations thereof can seemingly trigger a critical lack of oxygen in brain tissue, and the restoration of capillary perfusion patterns therefore appears to be crucial for the restoration of the tissue oxygenation after ischemic episodes. In this review, we discuss the possible implications of these findings for the prevention, diagnosis, and treatment of acute stroke.

KW - Animals

KW - Humans

KW - Models, Biological

KW - Oxygen/metabolism

KW - Brain/blood supply/metabolism/physiopathology

KW - Brain Ischemia/diagnosis/metabolism/physiopathology/prevention & control

KW - Capillaries/metabolism/physiopathology

KW - Cerebrovascular Circulation

KW - Stroke/diagnosis/metabolism/physiopathology/prevention & control

KW - Animals

KW - Humans

KW - Models, Biological

KW - Oxygen/metabolism

KW - Brain/blood supply/metabolism/physiopathology

KW - Brain Ischemia/diagnosis/metabolism/physiopathology/prevention & control

KW - Capillaries/metabolism/physiopathology

KW - Cerebrovascular Circulation

KW - Stroke/diagnosis/metabolism/physiopathology/prevention & control

M3 - SCORING: Journal article

VL - 33

SP - 635

EP - 648

JO - J CEREBR BLOOD F MET

JF - J CEREBR BLOOD F MET

SN - 0271-678X

IS - 5

M1 - 5

ER -