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Postischemic Estrogen Reduces Hypoperfusion and Secondary Ischemia After Experimental Stroke
Abstract
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.
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 (n=15 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 (n=10) or 90 (n=11) minutes of reperfusion.
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 (n=15 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 (n=10) or 90 (n=11) minutes of reperfusion.
Results—
As expected, supraphysiological plasma estrogen levels were achieved during reperfusion (estrogen, 198±45 pg/mL; vehicle, 6±5; P=0.001). Physiological variables were controlled and not different between groups. Total hemispheric infarction was reduced in estrogen-treated rats (estrogen, 49±4% of ipsilateral structure; vehicle, 33±5%; P=0.02), which was most pronounced in striatum (estrogen, 40±6% of ipsilateral striatum; vehicle, 60±3%; P=0.01). CBF recovery was strikingly increased by estrogen infusion at 10 minutes in frontal (estrogen, 102±12 mL/100 g per minute; vehicle, 45±15; P=0.01) and parietal cortex (estrogen, 74±15 mL/100 g per minute; vehicle, 22±13; P=0.028) and throughout striatum (estrogen, 87±13 mL/100 g per minute; vehicle, 25±20; P=0.02). Hemispheric volume with low CBF recovery (eg, < 20 mL/100 g per minute) was smaller in estrogen-treated animals (estrogen, 73±18 mm3; vehicle, 257±46; P=0.002). However, differences in CBF recovery could not be appreciated between groups by 90 minutes of reperfusion.
As expected, supraphysiological plasma estrogen levels were achieved during reperfusion (estrogen, 198±45 pg/mL; vehicle, 6±5; P=0.001). Physiological variables were controlled and not different between groups. Total hemispheric infarction was reduced in estrogen-treated rats (estrogen, 49±4% of ipsilateral structure; vehicle, 33±5%; P=0.02), which was most pronounced in striatum (estrogen, 40±6% of ipsilateral striatum; vehicle, 60±3%; P=0.01). CBF recovery was strikingly increased by estrogen infusion at 10 minutes in frontal (estrogen, 102±12 mL/100 g per minute; vehicle, 45±15; P=0.01) and parietal cortex (estrogen, 74±15 mL/100 g per minute; vehicle, 22±13; P=0.028) and throughout striatum (estrogen, 87±13 mL/100 g per minute; vehicle, 25±20; P=0.02). Hemispheric volume with low CBF recovery (eg, < 20 mL/100 g per minute) was smaller in estrogen-treated animals (estrogen, 73±18 mm3; vehicle, 257±46; P=0.002). 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.
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