Estrogen restores postischemic pial microvascular dilation

Estrogen restores postischemic pial microvascular dilation Abstract Estrogen protects the brain from experimental cerebral ischemia, likely through both vascular and neuronal cellular mechanisms. The purpose of this study was to determine whether chronic estrogen treatment in males and repletion in ovariectomized (Ovx) females reverses abnormalities in pial arteriolar reactivity during reperfusion from global forebrain ischemia (4-vessel occlusion, 15 min) and whether the site of protection is vascular endothelium. Male and Ovx female rats were implanted with either placebo or a 25-μg 17β-estradiol pellet 10 days before ischemia. With the use of intravital microscopy, pial vessel dilation to ACh (10 μM) and S -nitroso- N -acetyl-penicillamine (SNAP; 1 μM) and vasoconstriction to serotonin (10 μM) was examined in situ at 30–60 min of reperfusion. Postischemic changes in vessel diameter were compared with preischemic values for each agent. Postischemic 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, suggesting that estrogen protects both endothelial and smooth muscle-mediated vasodilation. Ischemia blunted vessel constriction to serotonin regardless of treatment. These data demonstrate that estrogen acts as a vasoprotective agent within the cerebral circulation and can improve microvascular function under conditions of an acutely evolving ischemic pathology. cerebral ischemia microvasculature pial circulation Footnotes This work was supported in part by National Institutes of Health Grants NS-20020, NS-33668, NR-03521, and NR-04943. Address for reprint requests and other correspondence: M. T. Littleton-Kearney, 1508-B, Blalock, 600 N. Wolfe St., Baltimore, MD 21287 (E-mail: mkearney@jhmi.edu ). The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “ advertisement ” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. Copyright © 2001 the American Physiological Society http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Heart and Circulatory Physiology The American Physiological Society

Estrogen restores postischemic pial microvascular dilation

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Publisher
The American Physiological Society
Copyright
Copyright © 2011 the American Physiological Society
ISSN
0363-6135
eISSN
1522-1539
Publisher site
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Abstract

Abstract Estrogen protects the brain from experimental cerebral ischemia, likely through both vascular and neuronal cellular mechanisms. The purpose of this study was to determine whether chronic estrogen treatment in males and repletion in ovariectomized (Ovx) females reverses abnormalities in pial arteriolar reactivity during reperfusion from global forebrain ischemia (4-vessel occlusion, 15 min) and whether the site of protection is vascular endothelium. Male and Ovx female rats were implanted with either placebo or a 25-μg 17β-estradiol pellet 10 days before ischemia. With the use of intravital microscopy, pial vessel dilation to ACh (10 μM) and S -nitroso- N -acetyl-penicillamine (SNAP; 1 μM) and vasoconstriction to serotonin (10 μM) was examined in situ at 30–60 min of reperfusion. Postischemic changes in vessel diameter were compared with preischemic values for each agent. Postischemic 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, suggesting that estrogen protects both endothelial and smooth muscle-mediated vasodilation. Ischemia blunted vessel constriction to serotonin regardless of treatment. These data demonstrate that estrogen acts as a vasoprotective agent within the cerebral circulation and can improve microvascular function under conditions of an acutely evolving ischemic pathology. cerebral ischemia microvasculature pial circulation Footnotes This work was supported in part by National Institutes of Health Grants NS-20020, NS-33668, NR-03521, and NR-04943. Address for reprint requests and other correspondence: M. T. Littleton-Kearney, 1508-B, Blalock, 600 N. Wolfe St., Baltimore, MD 21287 (E-mail: mkearney@jhmi.edu ). The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “ advertisement ” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. Copyright © 2001 the American Physiological Society

Journal

AJP - Heart and Circulatory PhysiologyThe American Physiological Society

Published: Jul 1, 2001

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