Background and Purpose-Estrogen is a known neuroprotective and vasoprotective agent in experimental cerebral ischemia. Preischemic steroid treatment protects animals of both sexes from focal cerebral ischemia. This study determined whether intravenous estrogen acts as a vasodilator when administered on reperfusion and whether the resulting increase in cerebral blood flow (CBF) provides tissue protection from middle cerebral artery occlusion. Methods-Adult male Wistar rats were treated with reversible middle cerebral artery occlusion (2 hours), then infused with intravenous estrogen (Premarin; 1 mg/kg) or vehicle during the first minutes of reperfusion (nϭ15 per group). Cortical laser-Doppler flowmetry was used to assess adequacy of occlusion. Ischemic lesion volume was determined at 22 hours after occlusion by 2,3,5-triphenyltetrazolium chloride staining and image analysis. Cortical and striatal CBF was measured by 14 [C]iodoantipyrine autoradiography at 10 (nϭ10) or 90 (nϭ11) minutes of reperfusion. Results-As expected, supraphysiological plasma estrogen levels were achieved during reperfusion (estrogen, 198Ϯ45 pg/mL; vehicle, 6Ϯ5; Pϭ0.001). Physiological variables were controlled and not different between groups. Total hemispheric infarction was reduced in estrogen-treated rats (estrogen, 49Ϯ4% of ipsilateral structure; vehicle, 33Ϯ5%; Pϭ0.02), which was most pronounced in striatum (estrogen, 40Ϯ6% of ipsilateral striatum; vehicle, 60Ϯ3%; Pϭ0.01). CBF recovery was strikingly increased by estrogen infusion at 10 minutes in frontal (estrogen, 102Ϯ12 mL/100 g per minute; vehicle, 45Ϯ15; Pϭ0.01) and parietal cortex (estrogen, 74Ϯ15 mL/100 g per minute; vehicle, 22Ϯ13; Pϭ0.028) and throughout striatum (estrogen, 87Ϯ13 mL/100 g per minute; vehicle, 25Ϯ20; Pϭ0.02). Hemispheric volume with low CBF recovery (eg, Ͻ20 mL/100 g per minute) was smaller in estrogen-treated animals (estrogen, 73Ϯ18 mm 3 ; vehicle, 257Ϯ46; Pϭ0.002). However, differences in CBF recovery could not be appreciated between groups by 90 minutes of reperfusion. Conclusions-Acute estrogen therapy during reperfusion improves tissue outcome from experimental stroke. The steroid rapidly promotes CBF recovery and reduces hemispheric no-reflow zones. This beneficial effect appears only during early reperfusion and likely complements other known mechanisms by which estrogen salvages brain from focal necrosis. Key Words: cerebral ischemia, focal Ⅲ estrogens Ⅲ gender Ⅲ middle cerebral artery occlusion Ⅲ reperfusion Ⅲ stroke, acute Ⅲ women E strogen has been widely shown to protect brain in numerous models of experimental brain injury. Preischemic steroid treatment has been well studied as a neuroprotective agent in adult animals of both sexes and in reproductively senescent, middle-aged female rats (for reviews, see 1, 2). From the perspective of cerebrovascular disease and stroke, estrogen has been primarily of interest as a postmenopausal hormone therapy that could reduce stroke incidence. The therapeutic utility of the steroid in postischemic treatment p...

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This MRI cartilage score demonstrated excellent reliability when tested in a three-reader system. However, cartilage loss in early RA could not be distinguished from that seen in healthy controls.