Hatashita T, Ito M, Miyaoka M, Ishii S
Department of Neurosurgery, School of Medicine, Juntendo University, Tokyo, Japan.
Adv Neurol. 1990;52:29-37.
The chronological changes of ischemic brain edema, rCBF, and LCGU were examined in SHR and WKY 6, 24, and 48 hr after MCAO. The analysis focused on the ischemic periphery in the cortex at the level of caudate nucleus. The ischemic areas in the cortex as identified on stained sections were more extensive in rats with hypertension than in those with normotension. The swelling of the ischemic hemisphere progressed until 48 hr after MCAO in hypertension; however, the peak of brain swelling was found at 24 hr in normotension and then resolved 48 hr after MCAO. The water content was also increased in hypertension at 48 hr after MCAO. Determination of rCBF and LCGU was made by a double-label autoradiographic method using [14C]deoxyglucose and [14C]iodoantipyrine. In the early period (6 hr) after MCAO, the reduction of rCBF was greater than the reduction of LCGU in both hypertension and normotension, indicating misery perfusion. After 24 and 48 hr of MCAO, the rCBF and LCGU recovered in normotension; however, the progressive reductions in rCBF and LCGU were observed in hypotension. These results suggest that an increased hydrostatic pressure gradient in the ischemic periphery may play an important role in the development of edema and impairment in both rCBF and LCGU.