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CO(2) reactivity measured by perfusion MRI during transient focal cerebral ischemia in rats
1Max-Planck-Institute for Neurological Research, Department of Experimental Neurology, Cologne, Germany.
Background And Purpose:
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.
Insights
Carbon dioxide (CO2) response, a measure of vascular reactivity, remains impaired long after cerebral ischemia and reperfusion, even when tissue energy metabolism normalizes. This study investigated CO2 response in ischemic and recovered brain tissues in rats.
Area of Science:
- Neuroscience
- Medical Imaging
- Cerebrovascular Research
Background:
- Middle cerebral artery occlusion (MCAO) is a model for studying cerebral ischemia.
- Vascular reactivity, assessed by CO2 response, is crucial for maintaining cerebral blood flow.
- The recovery of CO2 response after ischemia and reperfusion is not well understood.
Purpose of the Study:
- To investigate the spatially resolved CO2 response in rats after MCAO and reperfusion.
- To determine if vascular reactivity recovers in parallel with tissue recovery.
- To differentiate CO2 response in permanently damaged versus recovered ischemic brain areas.
Main Methods:
- Diffusion-weighted magnetic resonance imaging (MRI) was used to calculate apparent diffusion coefficient (ADC) maps.
- CO2 reactivity maps were generated by measuring perfusion signal changes in response to CO2 inhalation.
- Adenosine triphosphate (ATP) levels were measured to assess tissue outcome and differentiate damaged from recovered areas.
Main Results:
- CO2 reactivity significantly decreased during MCAO.
- During reperfusion, CO2 reactivity remained severely impaired in areas with significant tissue damage (ADC <80% of control).
- A gradual recovery of CO2 reactivity was observed in less affected areas (ADC >80% of control), but remained below normal levels.
Conclusions:
- Noninvasive perfusion-weighted MRI with CO2 challenge allows longitudinal assessment of vascular reactivity in cerebral ischemia.
- Severe cerebral ischemia leads to prolonged disturbance of CO2 reactivity, even with normalized energy metabolism.
- Vascular dysfunction persists despite apparent tissue recovery, highlighting the complexity of post-ischemic brain healing.