Paper
Thursday, July 22, 2004
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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