Acute changes in neurovascular reactivity after subarachnoid hemorrhage in vivo.

Autor: Balbi M; Institute for Stroke and Dementia Research (ISD), University of Munich Medical Center, Munich, Germany.; Graduate School of Systemic Neurosciences (GSN), Ludwig-Maximilians University (LMU), Munich, Germany., Koide M; Department of Pharmacology, University of Vermont, Burlington, VT, USA., Schwarzmaier SM; Institute for Stroke and Dementia Research (ISD), University of Munich Medical Center, Munich, Germany., Wellman GC; Department of Pharmacology, University of Vermont, Burlington, VT, USA., Plesnila N; Institute for Stroke and Dementia Research (ISD), University of Munich Medical Center, Munich, Germany nikolaus.plesnila@med.uni-muenchen.de.; Graduate School of Systemic Neurosciences (GSN), Ludwig-Maximilians University (LMU), Munich, Germany.; Munich Cluster for Systems Neurology, Munich, Germany.
Jazyk: angličtina
Zdroj: Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism [J Cereb Blood Flow Metab] 2017 Jan; Vol. 37 (1), pp. 178-187. Date of Electronic Publication: 2015 Dec 16.
DOI: 10.1177/0271678X15621253
Abstrakt: Subarachnoid hemorrhage causes acute and long-lasting constrictions of pial arterioles. Whether these vessels dilate normally to neuronal activity is of great interest since a mismatch between delivery and consumption of glucose and oxygen may cause additional neuronal damage. Therefore, we investigated neurovascular reactivity of pial and parenchymal arterioles after experimental subarachnoid hemorrhage. C57BL/6 mice were subjected to subarachnoid hemorrhage by filament perforation or sham surgery. Neurovascular reactivity was assessed 3 h later by forepaw stimulation or inhalation of 10% CO 2 Diameters of cerebral arterioles were assessed using two-photon microscopy. Neurovascular coupling and astrocytic endfoot Ca 2+ were measured in brain slices using two-photon and infrared-differential interference contrast microscopy. Vessels of sham-operated mice dilated normally to CO 2 and forepaw stimulation. Three hours after subarachnoid hemorrhage, CO 2 reactivity was completely lost in both pial and parenchymal arterioles, while neurovascular coupling was not affected. Brain slices studies also showed normal neurovascular coupling and a normal increase in astrocytic endfoot Ca 2+ acutely after subarachnoid hemorrhage. These findings suggest that communication between neurons, astrocytes, and parenchymal arterioles is not affected in the first few hours after subarachnoid hemorrhage, while CO 2 reactivity, which is dependent on NO signaling, is completely lost.
(© The Author(s) 2015.)
Databáze: MEDLINE
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