Ahead of print ID: ERMPS-12004

DWI and PWI studies in New Zealand rabbit model of acute cerebral infarction treated by delayed thrombolysis

P. Jin, H.-T. Huang, J.-Z. Gu, Q. Qian, S. Chen, S.-D. He, L. Xu, M. Lin

Department of Radiology, The Third Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang Province, China. minlin160817@163.com


OBJECTIVE: To identify the varying patterns of diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) over time in different areas of acute cerebral infarction in New Zealand rabbit model treated with delayed thrombolysis.

MATERIALS AND METHODS: New Zealand rabbits (n = 50) were used to establish a successful model of acute cerebral infarction treated with delayed thrombolysis using MRI over different time periods. The changes in rADC, rNEI, rTTM and rMSI were analyzed and the changes in the high signal area of DWI at different time points after the onset of acute cerebral infarction were examined using electron microscopy.

RESULTS: Decreases in rADC, rNEI, rMSI and the prolongation of rTTM were detected in different parts in the acute cerebral infarction, while the signal was significantly higher in the central area than in the marginal area. On day 1, no significant change was observed in rADC of central area, but since day 2, a gradual increase of rADC was observed in central area; 12h after onset of cerebral infarction, the rADC in marginal area was first gradually decreased to 76%, the lowest point, and then gradually increased to the same level of the corresponding contralateral area after day 10. Significant differences were found in the comparison of signals in 0.5-1.5h and 9-24h after the onset of cerebral infarction between the central area and the marginal area (p < 0.05). Similar change patterns were identified in rNEIs of the central area and marginal area, 18.12% and 51.36%, respectively. On day 1 after the onset of cerebral infarction, the rNEIs in the central area and marginal area, with the extension in time of cerebral infarction, were found to be significantly different from each other in different time point (p < 0.05). After the onset of cerebral infarction, rTTM was gradually shortened, and rMSI was decreased initially and then increased gradually within 4h. Intersection and overlapping parts were found between rTTM and rMSI in the central area and the marginal area of cerebral infarction at different time points. Using electron microscopy, diversified characteristics were identified in the high signal area of the DWI at different time point after acute cerebral infarction.

CONCLUSIONS: Dynamic observation of the evolution patterns of DWI and PWI of New Zealand rabbit models of acute cerebral infarction treated with delayed thrombolysis can contribute to the understanding of the changes in the blood flow and the pathophysiology in different areas of acute cerebral infarction, thus providing individualized information for the selection of therapeutic time window for delayed thrombolysis.