title: CO(2) reactivity measured by perfusion MRI during transient focal cerebral ischemia in rats.
abstract: OBJECTIVE
  CO(2) 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, CO(2) 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 CO(2) reactivity maps were determined from the difference in perfusion signal intensity before and after CO(2) stimulation. CO(2) reactivity (administration of 6% CO(2) for 5 minutes) was expressed in % change of perfusion signal intensity/mm Hg of PCO(2) 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) CO(2) 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 CO(2) 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 CO(2) 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 CO(2) reactivity, despite already normalized energy metabolism.
authors.affiliation: Max-Planck-Institute for Neurological Research, Department of Experimental Neurology, Cologne, Germany.
authors.forename: L
authors.initials: L
authors.lastname: Olah
authors.forename: C
authors.initials: C
authors.lastname: Franke
authors.forename: W
authors.initials: W
authors.lastname: Schwindt
authors.forename: M
authors.initials: M
authors.lastname: Hoehn
mesh_terms: D000255:Adenosine Triphosphate / Q000032:analysis; D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism* / Q000473:pathology; D002245:Carbon Dioxide / Q000032:analysis / Q000378:metabolism* / Q000494:pharmacology; D004058:Diffusion; D004734:Energy Metabolism; D008163:Luminescent Measurements; D008279:Magnetic Resonance Imaging / Q000379:methods; D008297:Male; D020768:Middle Cerebral Artery / Q000378:metabolism; D011699:Putamen / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D015424:Reperfusion; D013997:Time Factors
chemical_list: D002245:Carbon Dioxide; D000255:Adenosine Triphosphate