Related Experiment Video
Updated: Aug 15, 2025

Middle Cerebral Artery Occlusion Allowing Reperfusion via Common Carotid Artery Repair in Mice
Published on: January 23, 2019
Heterogeneity evaluation of multi-high b-value apparent diffusion coefficient on cerebral ischemia in MCAO rat
Liwei Shi1,2,3, Bo Yu2,3, Qiuyan Chen2,3
1The Third Clinical Medical College, Fujian Medical University, Fuzhou, Fujian, China.
Purpose:
To assess brain damage in a rat model of cerebral ischemia based on apparent diffusion coefficient (ADC) data obtained from multi-high b-values and evaluate the relationship between Aquaporin 4 (AQP4) expression and ADC.
Methods:
Thirty eight male Sprague-Dawley rats were randomized into two groups: (1) sham controls (n = 6) and (2) cerebral ischemia (successful model, n = 19). All rats underwent diffusion-weighted imaging (DWI) with both standard b-values and multi-high b-values (2,500-4,500 s/mm2) using a 3.0-T device. Standard ADC (ADCst) maps and multi-high b-value ADCs (ADCmh) were calculated, respectively. Aquaporin 4 expression was quantified using Western blot. Relative values of ADCst and ADCmh, AQP4 expression were compared between the sham group and the ischemia group. Correlations between ADC values and AQP4 expression were evaluated.
Results:
At 0.5 h after suture insertion, the value of ADCmh on the lesion was obviously decreased, and there was no difference in lesion volume when compared with ADCst. After reperfusion, besides similar regions where ADCst values decreased, we also found additional large values on ADCmh within the cortex of the ipsilateral side or surrounding the lesion. The lesion evolution of the large value on ADCmh was quite different from other indicators. But the total ADCmh values were still significantly associated with ADCst. The AQP4 protein expression level was appreciably increased after middle cerebral artery occlusion (MCAO), but there was no correlation between AQP4 expression either with ADCmh or ADCst.
Conclusion:
We found the large values on ADCmh during the progression of cerebral infarction is varied, but there was no correlation between ADCmh values and AQP4 expression. ADCmh may indicate the heterogeneity of ischemia lesions, but the underlying pathological basis should be further explored.
Insights
Multi-high b-value diffusion-weighted imaging (DWI) revealed varied apparent diffusion coefficient (ADC) values during cerebral infarction progression in rats. However, these ADC values did not correlate with Aquaporin 4 (AQP4) expression, suggesting further research is needed.
Area of Science:
- Neuroscience
- Radiology
- Biochemistry
Background:
- Cerebral ischemia can cause significant brain damage.
- Diffusion-weighted imaging (DWI) is a key tool for assessing brain tissue changes.
- Apparent diffusion coefficient (ADC) values derived from DWI can quantify these changes.
Purpose of the Study:
- To evaluate brain damage in a rat model of cerebral ischemia using multi-high b-value ADC data.
- To investigate the relationship between Aquaporin 4 (AQP4) expression and ADC values in this model.
Main Methods:
- A rat model of cerebral ischemia was established.
- Diffusion-weighted imaging (DWI) was performed using standard and multi-high b-values (2,500-4,500 s/mm²).
- Apparent diffusion coefficient (ADC) maps (ADCst and ADCmh) were calculated, and Aquaporin 4 (AQP4) expression was measured via Western blot.
Main Results:
- Multi-high b-value ADC (ADCmh) showed decreased values at the lesion site early after ischemia and distinct patterns during reperfusion compared to standard ADC (ADCst).
- Despite differences, total ADCmh values remained associated with ADCst values.
- Aquaporin 4 (AQP4) protein expression increased after middle cerebral artery occlusion (MCAO), but showed no correlation with either ADCmh or ADCst.
Conclusions:
- Multi-high b-value ADC (ADCmh) values exhibited variability during cerebral infarction progression.
- No correlation was found between ADCmh values and Aquaporin 4 (AQP4) expression.
- ADCmh may reflect lesion heterogeneity in cerebral ischemia, but its pathological basis requires further investigation.

