Paper
Thursday, July 22, 2004
This presentation is part of : Critical-Care Nursing
Estrogen Status Effects Post-Ischemic Pial Vascular Responses to Vasoconstrictors
Marguerite T. Littleton-Kearney, DNSc, RN, FAAN, Johns Hopkins University School of Nursing, Baltimore, MD, USA, Xinyue Quin, MD, PhD, Anesthesia/Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA, and Patricia D. Hurn, PhD, RN, Anesthesiology and Perioperative Medicine, Oregon Health Science sUniversity, Portland, OR, USA.
Learning Objective #1: Describe the effects of estrogen depletion and repletion on post-ischemic pial arterial responses to the vasoconstrictor U46619
Learning Objective #2: Compare and contrast pre-and post-ischemic responses to U46619 in the presence and the absence of a pure estrogen receptor inhibitor

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

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