Summary
This study was performed to test whether 17β-estradiol could attenuate the blood-brain
barrier disruption caused by middle cerebral artery occlusion in the ovariectomized
rats. Rats aged twelve to fourteen weeks were used in this study. Their ovaries were
removed one week prior to the implantation of the pellets. For the 17β-estradiol group,
a 500 µg 17β-estradiol 21 day-release pellet was implanted and for the control group,
a vehicle pellet was implanted 21 days before the experiments. One hour after middle
cerebral artery occlusion under isoflurane anesthesia, the transfer coefficient of
14 C-α-aminoisobutyric acid (104 Daltons) and the volume of 3 H-dextran (70 000 Daltons) distribution were determined to represent the degree of
blood-brain barrier disruption. Blood pressures and blood gases were similar between
controls and 17β-estradiol-treated rats. In both groups, the transfer coefficient
of the ischemic cortex was higher than that of the corresponding contralateral cortex
(control: Ischemic Cortex 12.5 ± 5.9 µl/g/min, Contralateral Cortex 3.0 ± 1.6, p <
0.001; 17β-estradiol: Ischemic Cortex 6.7 ± 3.3 µl/g/min, Contralateral Cortex 2.2
± 0.9, p < 0.01). There was no significant difference in the transfer coefficient
of the contralateral cortex between these two groups. However, the transfer coefficient
of the Ischemic Cortex of the 17β-estradiol-treated animals was 46 % lower than that
of the control, vehicle-treated rats (p < 0.05). The increase of the volume of 3 H-dextran distribution with middle cerebral artery occlusion was significant in the
vehicle-treated rats (Ischemic Cortex: 6.4 ± 2.7 ml/100 g, Contralateral Cortex: 3.8
± 0.8, p < 0.01) but not in the 17β-estradiol-treated animals. Our data suggest that
chronic 17β-estradiol treatment was effective in reducing blood-brain barrier disruption
during focal ischemia in the ovariectomized rats.
Key words
Brain - Capillary Permeability - Estrogen - Stroke
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chi@umdnj.edu
