title: 17 beta-Estradiol prevents dysfunction of canine coronary endothelium and myocardium and reperfusion arrhythmias after brief ischemia/reperfusion.
abstract: BACKGROUND
  Brief myocardial ischemia is associated with myocardial and coronary endothelial dysfunction caused by oxygen free radicals released during reperfusion. Estrogen, known to have antioxidant activity, may prevent these complications.
  
  
  RESULTS
  We assessed the effect of 2 weeks of treatment with 17 beta-estradiol (E, 100 micrograms.kg-1.d-1, n = 12) or placebo (P, n = 15) on myocardial and coronary endothelial function during the first 2 hours of reperfusion in dogs subjected to 15 minutes of ischemia induced by occlusion of the left anterior descending coronary artery (LAD). Our results show that the incidence of ventricular arrhythmias significantly decreased in E (3 of 12) compared with P (11 of 15). Systolic shortening, significantly depressed in P during early reperfusion, was maintained at preischemic levels in E. During reperfusion, the increase in LAD flow to acetylcholine, attenuated in P (60 +/- 6%), was preserved in E endothelium. (151 +/- 28%) and was associated with increased serum nitrite/nitrate concentration. n-Pentane in exhaled gas in vivo, an index of lipid peroxidation, increased significantly during early reperfusion in P (from 9.1 +/- 1.9 to 41.6 +/- 13.0 ppb, P < .05) but not in E (23.0 +/- 6.9 ppb). In vitro, arterial segments from E generated significantly less superoxide anion after hypoxia/reoxygenation than those from P. Ischemic/reperfused LAD segments from E also revealed a better preservation of endothelium-dependent relaxation in vitro (maximum relaxation, 42 +/- 4% versus 24 +/- 4% in P; P < .05).
  
  
  CONCLUSIONS
  Estrogen protects against endothelial and myocardial dysfunction resulting from brief ischemia/reperfusion. This protection may relate to an antioxidant effect of estrogen.
authors.affiliation: Department of Anesthesia, Georgetown University Medical Center, Washington, DC 20007, USA.
authors.forename: Y D
authors.initials: YD
authors.lastname: Kim
authors.forename: B
authors.initials: B
authors.lastname: Chen
authors.forename: J
authors.initials: J
authors.lastname: Beauregard
authors.forename: P
authors.initials: P
authors.lastname: Kouretas
authors.forename: G
authors.initials: G
authors.lastname: Thomas
authors.forename: M Y
authors.initials: MY
authors.lastname: Farhat
authors.forename: A K
authors.initials: AK
authors.lastname: Myers
authors.forename: D E
authors.initials: DE
authors.lastname: Lees
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000517:prevention & control*; D003326:Coronary Circulation / Q000187:drug effects; D003331:Coronary Vessels / Q000187:drug effects / Q000503:physiopathology*; D004285:Dogs; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology*; D004958:Estradiol / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects / Q000503:physiopathology*; D006439:Hemodynamics; D008297:Male; D009200:Myocardial Contraction; D017202:Myocardial Ischemia / Q000150:complications*; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D009599:Nitroprusside / Q000494:pharmacology; D014664:Vasodilation; D014665:Vasodilator Agents / Q000494:pharmacology; D014666:Vasomotor System / Q000187:drug effects
chemical_list: D014665:Vasodilator Agents; D009599:Nitroprusside; D004958:Estradiol; D000109:Acetylcholine