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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
-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 PPT [4,4',4''-(4-propyl-(1H)-pyrazole-1,3,5-triyl)tris-phenol; ER] and DPN [2,3-bis(4-hydroxyphenyl)-propionitrile; ER] 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, but not ER, is required for the observed cardioprotective effects of E2.
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