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This Article Full Text Full Text (PDF) All Versions of this Article: 289/5/H2039    most recent 00479.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (37) Citing Articles via Google Scholar Google Scholar Articles by Booth, E. A. Articles by Lucchesi, B. R. Search for Related Content PubMed PubMed Citation Articles by Booth, E. A. Articles by Lucchesi, B. R.

Activation of estrogen receptor- protects the in vivo rabbit heart from ischemia-reperfusion injury

Department of Pharmacology, University of Michigan Medical School, Ann Arbor, Michigan

Submitted 10 May 2005 ; accepted in final form 24 June 2005

The estrogen receptor (ER) mediates estrogenic activity in a variety of organs, including those in the reproductive, cardiovascular, immune, and central nervous systems. Experimental studies have demonstrated that 17-estradiol (E2) protects the heart from ischemia-reperfusion injury. Two estrogen receptors, ER and ER, mediate the actions of estrogen; however, it is not certain which ER mediates the cardioprotective effects of E2. In the present study, the ER-selective agonists 4,4',4''-[4-propyl-(1H)-pyrazole-1,3,5-triyl]tris-phenol (PPT; ER) and 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN; ER) were assessed for their cardioprotective potential in an in vivo rabbit model of ischemia-reperfusion injury. Anesthetized female rabbits were administered PPT (3 mg/kg), DPN (3 mg/kg), E2 (20 µg/rabbit), or vehicle intravenously 30 min before a 30-min occlusion of the left anterior descending coronary artery followed by 4 h of reperfusion. Acute treatment with E2 (17.7 ± 2.9%; P < 0.001) and PPT (18.1 ± 2.9%; P < 0.001), but not DPN (45.3 ± 2.4%) significantly decreased infarct size as a percent of area at risk compared with vehicle (45.3 ± 2.4%). Coadministration of PPT or E2 with the ER antagonist ICI-182,780 limited the infarct size-sparing effect of the compounds (43.8 ± 6.6% and 40.6 ± 5.7% respectively, expressed as a percentage of risk region). PPT reduced the release of cardiac-specific troponin-I and reduced the tissue deposition of the membrane attack complex and C-reactive protein similar to that of E2. The results indicate that activation of ER, but not ER, is required for the observed cardioprotective effects of E2.

infarct size; membrane attack complex; C-reactive protein; estrogen; 4,4&",4&"-[4-propyl-(1H)-pyrazole-1,3,5-triyl]tris-phenol

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