The Role of the Microcirculation in Delayed Cerebral Ischemia and Chronic Degenerative Changes after Subarachnoid Hemorrhage

The mortality after aneurysmal subarachnoid hemorrhage (SAH) is 50%, and most survivors suffer severe functional and cognitive deficits. Half of SAH patients deteriorate 5 to 14 days after the initial bleeding, so-called delayed cerebral ischemia (DCI). Although often attributed to vasospasms, DCI m...

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Bibliographic Details
Published in:	Journal of Cerebral Blood Flow & Metabolism Vol. 33; no. 12; pp. 1825 - 1837
Main Authors:	Østergaard, Leif, Aamand, Rasmus, Karabegovic, Sanja, Tietze, Anna, Blicher, Jakob Udby, Mikkelsen, Irene Klærke, Iversen, Nina Kerting, Secher, Niels, Engedal, Thorbjørn Søndergaard, Anzabi, Mariam, Jimenez, Eugenio Gutierrez, Cai, Changsi, Koch, Klaus Ulrik, Næss-Schmidt, Erhard Trillingsgaard, Obel, Annette, Juul, Niels, Rasmussen, Mads, Sørensen, Jens Christian Hedemann
Format:	Book Review Journal Article
Language:	English
Published:	London, England SAGE Publications 01-12-2013 Sage Publications Ltd Nature Publishing Group
Subjects:	Aneurysm Brain - blood supply Brain - metabolism Brain - pathology Brain - physiopathology Brain Ischemia - complications Brain Ischemia - metabolism Brain Ischemia - pathology Brain Ischemia - physiopathology Humans Microcirculation Microvessels - metabolism Microvessels - pathology Microvessels - physiopathology Review Subarachnoid Hemorrhage - complications Subarachnoid Hemorrhage - metabolism Subarachnoid Hemorrhage - pathology Subarachnoid Hemorrhage - physiopathology capillary transit time heterogeneity vasospasm edema delayed cerebral ischemia microcirculation subarachnoid hemorrhage
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Summary:	The mortality after aneurysmal subarachnoid hemorrhage (SAH) is 50%, and most survivors suffer severe functional and cognitive deficits. Half of SAH patients deteriorate 5 to 14 days after the initial bleeding, so-called delayed cerebral ischemia (DCI). Although often attributed to vasospasms, DCI may develop in the absence of angiographic vasospasms, and therapeutic reversal of angiographic vasospasms fails to improve patient outcome. The etiology of chronic neurodegenerative changes after SAH remains poorly understood. Brain oxygenation depends on both cerebral blood flow (CBF) and its microscopic distribution, the so-called capillary transit time heterogeneity (CTH). In theory, increased CTH can therefore lead to tissue hypoxia in the absence of severe CBF reductions, whereas reductions in CBF, paradoxically, improve brain oxygenation if CTH is critically elevated. We review potential sources of elevated CTH after SAH. Pericyte constrictions in relation to the initial ischemic episode and subsequent oxidative stress, nitric oxide depletion during the pericapillary clearance of oxyhemoglobin, vasogenic edema, leukocytosis, and astrocytic endfeet swelling are identified as potential sources of elevated CTH, and hence of metabolic derangement, after SAH. Irreversible changes in capillary morphology and function are predicted to contribute to long-term relative tissue hypoxia, inflammation, and neurodegeneration. We discuss diagnostic and therapeutic implications of these predictions.
Bibliography:	ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 ObjectType-Feature-1
ISSN:	0271-678X 1559-7016
DOI:	10.1038/jcbfm.2013.173