MRI analysis of the changes in apparent water diffusion coefficient, T-2 relaxation time, and cerebral blood flow and volume in the temporal evolution of cerebral infarction following permanent middle cerebral artery occlusion in rats
M. Rudin et al., MRI analysis of the changes in apparent water diffusion coefficient, T-2 relaxation time, and cerebral blood flow and volume in the temporal evolution of cerebral infarction following permanent middle cerebral artery occlusion in rats, EXP NEUROL, 169(1), 2001, pp. 56-63
Detailed knowledge of similarities and differences between animal models an
d human stroke is decisive for selecting clinically effective drugs based o
n efficacy data obtained preclinically. Differences in the temporal evoluti
on of stroke pathologies between animal models and man have been reported.
In view of the importance of this issue for the development of neuroprotect
ive treatments, the temporal evolution of stroke pathologies in the rat per
manent middle cerebral artery occlusion (pMCAO) model has been evaluated wi
th magnetic resonance imaging modalities under experimental conditions matc
hing as close as possible those used in humans. Changes in the ipsilateral
and contralateral cortex and striatum of cerebral blood flow (CBF) and volu
me (CBV), apparent diffusion coefficient (ADC), and spin-spin relaxation ti
me (T-2), as well as total cortical and striatal infarct volumes, calculate
d from CBF, ADC, and T-2 maps, were determined starting 1 h up to 216 h pos
t-pMCAO. The temporal evolution of the MRI parameters in this rat model was
similar to that observed in humans. In particular, the ADC values were dec
reased for more than 3 days and returned back to baseline between 4 to 8 da
ys, to increase by day 9 only. Thus the stroke pathology in this rat model
develops at a similar pace as in stroke patients arguing against a fundamen
tal difference in the mechanisms involved. The infarct volumes however deve
lop differently in this rat model as they invariably increase over the firs
t 48 h, while in humans the evolution of infarct volume is slower and more
heterogeneous. (C) 2001 Academic Press.