Logo Logo
Help
Contact
Switch Language to German

Balbil, Matilde; Vega, Max Jativa; Lourbopoulos, Athanasios; Terpolilli, Nicole A. and Plesnila, Nikolaus (2019): Long-term impairment of neurovascular coupling following experimental subarachnoid hemorrhage. In: Journal of Cerebral Blood Flow and Metabolism, Vol. 40, No. 6: pp. 1193-1202 [PDF, 1MB]

[thumbnail of balbi-et-al-2019-long-term-impairment-of-neurovascular-coupling-following-experimental-subarachnoid-hemorrhage.pdf]
Preview

Download (1MB)

Abstract

CO2-reactivity and neurovascular coupling are sequentially lost within the first 24 h after subarachnoid hemorrhage (SAH). Whether and when these impairments recover is not known. Therefore, we investigated the reactivity of pial and intraparenchymal vessels by in vivo two-photon microscopy one month after experimental SAH. C57BL/6 mice were subjected to either sham surgery or SAH by filament perforation. One month later, cerebral blood flow following CO2-challenge and forepaw stimulation was assessed by laser Doppler fluxmetry. Diameters of pial and intraparenchymal arterioles were quantified by in vivo two-photon microscopy. One month after SAH, pial and parenchymal vessels dilated in response to CO2. Neurovascular coupling was almost completely absent after SAH: vessel diameter did not change upon forepaw stimulation compared to a 20% increase in sham-operated mice. The current results demonstrate that neurovascular function differentially recovers after SAH: while CO2-reactivity normalizes within one month after SAH, neurovascular coupling is still absent. These findings show an acute and persistent loss of neurovascular coupling after SAH that may serve as a link between early brain injury and delayed cerebral ischemia, two distinct pathophysiological phenomena after SAH that were so far believed not to be directly related.

Actions (login required)

View Item View Item