Secondary deterioration of apparent diffusion coefficient after 1-hour transient focal cerebral ischemia in rats

Oláh, László and Wecker, S. and Hoehn, M. (2000) Secondary deterioration of apparent diffusion coefficient after 1-hour transient focal cerebral ischemia in rats. JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 20 (10). pp. 1474-1482. ISSN 0271-678X

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Abstract

Recent investigations on transient focal cerebral ischemia suggested recovery of energy metabolism during early reperfusion, but followed by secondary energy failure. As disturbances of energy metabolism are reflected by changes of the apparent diffusion coefficient (ADC) of water, the aim of the current study was to follow the dynamics of the ADC during 1 hour of middle cerebral artery occlusion (MCAO) and 10 hours of reperfusion. The right MCA was occluded in male Wistar rats inside the magnet using a remotely controlled thread occlusion model. Diffusion-, perfusion-, and T2-weighted images were performed repetitively, and ADC, perfusion, and T2 maps were calculated and normalized to the respective preischemic value. The lesion volume at each time point was defined by ADC < 80% of control. At the end of 1-hour MCAO the hemispheric lesion volume was 22.3 ± 9.0%; it decreased to 6.4 ± 5.7% in the first 2 hours of reperfusion (P < 0.01), but then increased again, and by the end of 10 hours of reperfusion reached 17.3 ± 9.3%. The mean relative ADC in the end ischemic lesion volume significantly improved within 2 hours of reperfusion (from 65.7 ± 1.2% to 90.1 ± 6.7% of control), but later declined and decreased to 75.4 ± 7.3% of control by the end of the experiment. Pixels with secondary deterioration of ADC showed a continuous increase of T2 value during the first 2 hours of reperfusion in spite of ADC improvement, indicating improving cytotoxic, but generation of vasogenic edema during early reperfusion. A significant decrease of the perfusion level was not observed during 10 hours of recirculation. The authors conclude that the improvement of ADC in the early phase of reperfusion may be followed by secondary deterioration that was not caused by delayed hypoperfusion.

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