Estrogen restores postischemic pial microvascular dilation

Estrogen protects the brain from experimental cerebral ischemia, likely thr ough both vascular and neuronal cellular mechanisms. The purpose of this st udy was to determine whether chronic estrogen treatment in males and replet ion in ovariectomized (Ovx) females reverses abnormalities in pial arteriol ar reactivity during reperfusion from global forebrain ischemia (4-vessel o cclusion, 15 min) and whether the site of protection is vascular endotheliu m. Male and Ovx female rats were implanted with either placebo or a 25-mug 17 beta -estradiol pellet 10 days before ischemia. With the use of intravit al microscopy, pial vessel dilation to ACh (10 muM) and S-nitroso-N-acetyl- penicillamine (SNAP; 1 mM) and vasoconstriction to serotonin (10 muM) was e xamined in situ at 30-60 min of reperfusion. Postischemic changes in vessel diameter were compared with preischemic values for each agent. Postischemi c response to both ACh and SNAP was lost in males and Ovx females, but not in estrogen pellet-implanted males and estrogen-implanted Ovx females, sugg esting that estrogen protects both endothelial and smooth muscle-mediated v asodilation. Ischemia blunted vessel constriction to serotonin regardless o f treatment. These data demonstrate that estrogen acts as a vasoprotective agent within the cerebral circulation and can improve microvascular functio n under conditions of an acutely evolving ischemic pathology.