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Am J Physiol Heart Circ Physiol (July 1, 2005). doi:10.1152/ajpheart.00479.2005
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Submitted on May 10, 2005
Accepted on June 24, 2005

Activation of Estrogen Receptor alpha Protects the in vivo Rabbit Heart from Ischemia-Reperfusion Injury

Erin A Booth1, Nabeel R Obeid1, and Benedict R Lucchesi1*

1 Pharmacology, University of Michigan Medical School, Ann Arbor, MI, USA

* To whom correspondence should be addressed. E-mail: benluc{at}umich.edu.

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{beta}-estradiol (E2) protects the heart from ischemia-reperfusion injury. Two estrogen receptors, ER{alpha} and ER{beta}, 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 PPT [4,4',4''-(4-propyl-(1H)-pyrazole-1,3,5-triyl)tris-phenol; ER{alpha}] and DPN [2,3-bis(4-hydroxyphenyl)-propionitrile; ER{beta}] were assessed for their cardioprotective potential in an in vivo rabbit model of ischemia-reperfusion injury. Anesthetized female rabbits were administered PPT (3mg/kg), DPN (3mg/kg), E2 (20µg/rabbit), or vehicle intravenously 30 minutes before a 30 minute occlusion of the left anterior descending coronary artery followed by 4 hours 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 when compared to vehicle (45.3 ± 2.4). Co-administration 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 percent 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{alpha}, but not ER{beta}, is required for the observed cardioprotective effects of E2.




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