title: Acute changes in neurovascular reactivity after subarachnoid hemorrhage in vivo.
abstract: 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% CO2Diameters of cerebral arterioles were assessed using two-photon microscopy. Neurovascular coupling and astrocytic endfoot Ca2+were measured in brain slices using two-photon and infrared-differential interference contrast microscopy. Vessels of sham-operated mice dilated normally to CO2and forepaw stimulation. Three hours after subarachnoid hemorrhage, CO2reactivity 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 Ca2+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 CO2reactivity, which is dependent on NO signaling, is completely lost.
authors.affiliation: 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.
authors.forename: Matilde
authors.initials: M
authors.lastname: Balbi
authors.affiliation: Department of Pharmacology, University of Vermont, Burlington, VT, USA.
authors.forename: Masayo
authors.initials: M
authors.lastname: Koide
authors.affiliation: Institute for Stroke and Dementia Research (ISD), University of Munich Medical Center, Munich, Germany.
authors.forename: Susanne M
authors.initials: SM
authors.lastname: Schwarzmaier
authors.affiliation: Department of Pharmacology, University of Vermont, Burlington, VT, USA.
authors.forename: George C
authors.initials: GC
authors.lastname: Wellman
authors.affiliation: 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.
authors.forename: Nikolaus
authors.initials: N
authors.lastname: Plesnila
mesh_terms: D000818:Animals; D001160:Arterioles / Q000473:pathology / Q000503:physiopathology*; D001253:Astrocytes / Q000502:physiology; D002118:Calcium / Q000378:metabolism; D002245:Carbon Dioxide / Q000097:blood; D002450:Cell Communication; D051379:Mice; D008810:Mice, Inbred C57BL; D009474:Neurons / Q000502:physiology; D000069336:Neurovascular Coupling / Q000502:physiology*; D013345:Subarachnoid Hemorrhage / Q000503:physiopathology*; D013997:Time Factors; D014661:Vasoconstriction
chemical_list: D002245:Carbon Dioxide; D002118:Calcium
keywords: CO2; Subarachnoid hemorrhage; in vivo; neurovascular coupling; parenchymal vessels