CO ₂ Reactivity Measured by Perfusion MRI During Transient Focal Cerebral Ischemia in Rats

Abstract

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 3.5Ϯ0.9%/mm Hg decreased dramatically during MCAO in the ischemic hemisphere. During reperfusion, it remained Ͻ1%/mm Hg in the region with end-ischemic ADC Ͻ80% of the preischemic control value, but showed gradual recovery in the region with end-ischemic ADC Ͼ80% 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 (1.15Ϯ0.44 and 0.13Ϯ0.47%/mm Hg, respectively; PϽ0.01), it still remained far below the normal control value (PϽ0.01). 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. (Stroke. 2000;31:2236-2244.)

Quantification of rodent cerebral blood flow (CBF) in normal and high flow states using pulsed arterial spin labeling magnetic resonance imaging

“…The hippocampus, especially the cornu ammonis area 1 (CA1) subregion, is known for its susceptibility to ischemia (41) and low capillary density (42), with a low basal blood flow rate (14). The attenuated increase in hippocampal CBF in response to hypercapnia is in line with previous observations using BOLD MRI (34), and might be an indicator for a lower basal vasoreactivity as one possible factor determining higher susceptibility to ischemic damage (43).…”

Serial Changes in Static and Dynamic Cerebral Autoregulation after Acute Ischaemic Stroke

“…In addition, the majority of previous studies has been more concerned with cerebral vasoreactivity, i.e. the response to CO 2 or acetazolamide, rather than CA [7, 8], and it is now increasingly accepted that CA and CR are in fact two distinct processes that may be dissociated [14]. …”

“…However, it is unknown whether dynamic CA remains impaired following cerebral infarction. Recent reports in animal models of cerebral ischaemia have suggested that despite normalisation of the cerebral metabolism after reperfusion, those areas with the most severe ischaemic damage have persistently impaired CR, whereas in less ischaemic areas CR gradually improves with time [8]. …”

Altered Cerebral Vasoregulation Predicts the Outcome of Patients with Partial Anterior Circulation Stroke

“…Classifying patients according to the BHI cut-off of 0.69 [25], only 1 out of 13 patients (8%) with impaired cerebrovascular reactivity had a good clinical recovery, obtained by 41 out of 57 patients (72%) with normal cerebrovascular reactivity.…”

“…Then, the correlation of higher values of BHI with good clinical recovery leads to consider the importance of general factors for cerebral blood flow regulation that, in turn, seem to be able to influencing the prognosis of patients with partial anterior circulation infarct. In the absence of major arterial severe stenosis, an impaired CVR may reflect an increased rigidity of the arteriolar walls [25] or a poor efficiency of collateral circulation [32] and has been associated with conditions related to an increased risk of stroke. In fact, decreased CVR has been observed in patients with hypertension, diabetes mellitus and smoking [33,34].…”