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(Stroke. 2000;31:2236.)
© 2000 American Heart Association, Inc.

Original Contributions

CO₂ Reactivity Measured by Perfusion MRI During Transient Focal Cerebral Ischemia in Rats

Laszlo Olah, MD; Claudia Franke, PhD; Wolfram Schwindt, MD Mathias Hoehn, PhD

From the Max-Planck-Institute for Neurological Research, Department of Experimental Neurology, Cologne, Germany.

Correspondence to PD Dr Mathias Hoehn, Max-Planck-Institut für Neurologische Forschung, Abteilung für Experimentelle Neurologie, Gleueler Str 50, D-50931 Köln, Germany. E-mail mathias{at}mpin-koeln.mpg.de

Background and Purpose—CO₂ response was examined in rats undergoing 60 minutes of middle cerebral artery occlusion (MCAO) and 4.5 hours of reperfusion. Because it is not clear whether the vasoreactivity improves during reperfusion in parallel with tissue recovery, CO₂ response was determined spatially resolved, sequentially in the initially ischemic but later recovered areas and in the permanently damaged areas.

Methods—Apparent diffusion coefficient (ADC) maps were calculated from diffusion-weighted images, whereas CO₂ reactivity maps were determined from the difference in perfusion signal intensity before and after CO₂ stimulation. CO₂ reactivity (administration of 6% CO₂ for 5 minutes) was expressed in % change of perfusion signal intensity/mm Hg of PCO₂ increase. ATP levels of tissue were used as a measure of outcome. The recovered and permanently damaged tissues were differentiated by combined use of end-ischemic ADC map and ATP image at the end of the experiment.

Results—The preischemic (control) CO₂ reactivity of 3.5±0.9%/mm Hg decreased dramatically during MCAO in the ischemic hemisphere. During reperfusion, it remained <1%/mm Hg in the region with end-ischemic ADC <80% of the preischemic control value, but showed gradual recovery in the region with end-ischemic ADC >80% of control. Although at the end of the experiment the CO₂ reactivity was significantly higher in the recovered tissue than in the permanently damaged tissue (1.15±0.44 and 0.13±0.47%/mm Hg, respectively; P<0.01), it still remained far below the normal control value (P<0.01).

Conclusions—The noninvasive perfusion-weighted MR imaging in combination with a CO₂ challenge permits the investigation of the spatially resolved vascular reactivity during a longitudinal study of cerebral ischemia. Our data suggest that severe ischemia is followed by a prolonged disturbance of CO₂ reactivity, despite already normalized energy metabolism.

Editorial Comment

Marc Fisher, MD, Guest Editor

University of Massachusetts Medical School, Worcester, Massachusetts