Estrogen Status Effects Post-Ischemic Pial Vascular Responses to Vasoconstrictors

2.50
Hdl Handle:
http://hdl.handle.net/10755/151669
Type:
Presentation
Title:
Estrogen Status Effects Post-Ischemic Pial Vascular Responses to Vasoconstrictors
Abstract:
Estrogen Status Effects Post-Ischemic Pial Vascular Responses to Vasoconstrictors
Conference Sponsor:Sigma Theta Tau International
Conference Year:2004
Conference Date:July 22-24, 2004
Author:Littleton-Kearney, Marguerite T., DNSc, RN, FAAN
P.I. Institution Name:Johns Hopkins University School of Nursing
Title:Associate Professor
Co-Authors:Xinyue Quin, MD, PhD; Patricia D. Hurn, PhD, RN
Objective: To determine if chronic estrogen(E) therapy modulates post-ischemic pial vasoconstrictive response after a cerebral ischemic insult, we examined brain surface pial artery reactivity to the thromboxane analog, U46619(1 mcM, 0.1 mcM, 0.01 mcM). Sample: Five groups of ovariectomized rats(OVX: n=6/grp); OVX,OVX plus chronic estrogen(E),OVX plus acute E,(AE),OVX plus chronic E plus 10 mcM estrogen receptor(ER) inhibitor ICI(CEI), and OVX plus acute E plus 10 mcM ICI(AEI). Design: Chronic E rats were implanted with slow-release E pellets (50 mcg), the acute E 0.25 mg/kg E were given i.p. immedately before ischemia. ICI was given in the window at a dose of 10 mcM. Methods: Rats were prepped 24 hr. before reversible forebrain ischemia (4 vessel occlusion: 4VO).The next day rats were anesthetized, intubated,cannulated (femoral artery and vein)and fitted with a closed cranial window. Ischemia was induced via 4VO for 30 min. followed by 60 min. reperfusion. Arterial blood gases,intra-window pressure and temperature were controlled. Vessel diameter was measured prior to and 20 minutes after superfusion of each concentration both before ischemia and during reperfusion. Findings: In the OVX group vasoconstriction to U46619 was depressed after ischemia (p<0.05) as compared to pre-ischemic responses. Chronic E therapy restored constrictive responses to U46619 (-33.79± 6.03 % pre-ischemic baseline, vs. -32.12± 5.54 % post-ischemic baseline )as did acute E(-30.34 ± 2.27 % pre-ischemic baseline vs. -32.12 ± 3.05% post-ischemic baseline). However, pial constrictive responses in the rats treated with ICI were depressed even with E treatment. Conclusions: Under ischemic conditions, vasoconstrictive, like vasodilatory, responses are reduced in the brain microvasculature and these responses can be modulated by E via interaction with the ER. Implications: Chronic estrogen therapy can be beneficial after cerebrovascular insult perhaps by preserving either endothelial or vascular smooth muscle health. Supported By: NR05339
Repository Posting Date:
26-Oct-2011
Date of Publication:
22-Jul-2004
Sponsors:
Sigma Theta Tau International

Full metadata record

DC FieldValue Language
dc.typePresentationen_GB
dc.titleEstrogen Status Effects Post-Ischemic Pial Vascular Responses to Vasoconstrictorsen_GB
dc.identifier.urihttp://hdl.handle.net/10755/151669-
dc.description.abstract<table><tr><td colspan="2" class="item-title">Estrogen Status Effects Post-Ischemic Pial Vascular Responses to Vasoconstrictors</td></tr><tr class="item-sponsor"><td class="label">Conference Sponsor:</td><td class="value">Sigma Theta Tau International</td></tr><tr class="item-year"><td class="label">Conference Year:</td><td class="value">2004</td></tr><tr class="item-conference-date"><td class="label">Conference Date:</td><td class="value">July 22-24, 2004</td></tr><tr class="item-author"><td class="label">Author:</td><td class="value">Littleton-Kearney, Marguerite T., DNSc, RN, FAAN</td></tr><tr class="item-institute"><td class="label">P.I. Institution Name:</td><td class="value">Johns Hopkins University School of Nursing</td></tr><tr class="item-author-title"><td class="label">Title:</td><td class="value">Associate Professor</td></tr><tr class="item-email"><td class="label">Email:</td><td class="value">mkearne2@son.jhmi.edu</td></tr><tr class="item-co-authors"><td class="label">Co-Authors:</td><td class="value">Xinyue Quin, MD, PhD; Patricia D. Hurn, PhD, RN</td></tr><tr><td colspan="2" class="item-abstract">Objective: To determine if chronic estrogen(E) therapy modulates post-ischemic pial vasoconstrictive response after a cerebral ischemic insult, we examined brain surface pial artery reactivity to the thromboxane analog, U46619(1 mcM, 0.1 mcM, 0.01 mcM). Sample: Five groups of ovariectomized rats(OVX: n=6/grp); OVX,OVX plus chronic estrogen(E),OVX plus acute E,(AE),OVX plus chronic E plus 10 mcM estrogen receptor(ER) inhibitor ICI(CEI), and OVX plus acute E plus 10 mcM ICI(AEI). Design: Chronic E rats were implanted with slow-release E pellets (50 mcg), the acute E 0.25 mg/kg E were given i.p. immedately before ischemia. ICI was given in the window at a dose of 10 mcM. Methods: Rats were prepped 24 hr. before reversible forebrain ischemia (4 vessel occlusion: 4VO).The next day rats were anesthetized, intubated,cannulated (femoral artery and vein)and fitted with a closed cranial window. Ischemia was induced via 4VO for 30 min. followed by 60 min. reperfusion. Arterial blood gases,intra-window pressure and temperature were controlled. Vessel diameter was measured prior to and 20 minutes after superfusion of each concentration both before ischemia and during reperfusion. Findings: In the OVX group vasoconstriction to U46619 was depressed after ischemia (p&lt;0.05) as compared to pre-ischemic responses. Chronic E therapy restored constrictive responses to U46619 (-33.79&plusmn; 6.03 % pre-ischemic baseline, vs. -32.12&plusmn; 5.54 % post-ischemic baseline )as did acute E(-30.34 &plusmn; 2.27 % pre-ischemic baseline vs. -32.12 &plusmn; 3.05% post-ischemic baseline). However, pial constrictive responses in the rats treated with ICI were depressed even with E treatment. Conclusions: Under ischemic conditions, vasoconstrictive, like vasodilatory, responses are reduced in the brain microvasculature and these responses can be modulated by E via interaction with the ER. Implications: Chronic estrogen therapy can be beneficial after cerebrovascular insult perhaps by preserving either endothelial or vascular smooth muscle health. Supported By: NR05339</td></tr></table>en_GB
dc.date.available2011-10-26T11:09:46Z-
dc.date.issued2004-07-22en_GB
dc.date.accessioned2011-10-26T11:09:46Z-
dc.description.sponsorshipSigma Theta Tau Internationalen_GB
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