2014 Volume 7 Issue 1 Pages 33a
Background: We previously reported that cortical spreading depression (CSD) drastically suppresses red blood cell (RBC) velocity and alters cerebral blood flow (CBF) and vessel diameter in cortical arteriole. It has been reported that CSD induces disruption of neurovascular and neurometabolic coupling.
Objective: To further understand mechanisms involved in the disturbance of microcirculation, reactivity to carbon dioxide (CO2) in RBC velocity flowing in intraparenchymal capillaries and CBF was measured before and after CSD passage.
Methods: To visualize blood vessels, we used Tie2-GFP transgenic mice (N=10), in which specifically vascular endothelial cells emit fluorescence. Under urethane anesthesia and artificial ventilation, RBC velocity was measured using a confocal laser-scanning microscope with high-speed camera (125 fps) and an original image analyzing system of KEIO-IS2 working on MATLAB through a cranial window installed on the temporo-parietal region of the cerebral cortex, along with CBF by laser Doppler flowmeter. CO2 reactivity was measured with 5% CO2 inhalation for 1min. CSD was induced by microapplication of 1M KCl through a tiny cranial hole posterior to the cranial window.
Results: RBC velocity was measured in 4 to 21 capillaries in each mouse. CO2 inhalation increased partial pressure of arterial CO2 by 14.1±3.9mmHg. During hypercapnia, CBF and RBC velocity averaged in each mouse increased by 14.1±11.3% and 17.7±19.0% with significant correlation between the increases (r=0.79, n=8). After CSD passage, increase in CBF and RBC velocity were reduced to 7.3±21.8% and 11.6±22.9%, respectively, and the correlation was lost (r= -0.15, n=11).
Conclusion: CSD attenuated CO2 reactivity in CBF and RBC velocity by different mechanism, probably due to impairment of neurovascular and neurometabolic coupling.