Abstract
Estrogen plays a cardioprotective role in female rat hearts subjected to ischemia/reperfusion injury. The its effects are, at least partially, associated with decreased cardiomyocyte contraction and increased expression of β2-adrenoceptor (β2-AR). We tested whether β2-AR could be involved in cardioprotection against ischemic damage and whether the roles of β2-AR were dependent on estrogenic environment. We first determined the effects of hypoxia/reoxygenation (H/R) on cardiomyocyte shortening in female rats. We then determined the roles of β2-AR in cardiomyocyte shortening, lactate dehydrogenase (LDH) release in culture medium, and cell death during hypoxia in isolated myocytes from female rats. We further determined the effects of estrogen on the roles of β2-AR during hypoxia. H/R induced short-term hibernation and stunning at the level of ventricular myocytes from normal female rats. Inhibition of β2-AR with ICI118,551 significantly elevated adrenergic contractile reserve, myocardial injury, and cell death in normal female rats during hypoxia, whereas ovariectomy (OVX) prominently enhanced myocyte contraction, myocardial injury, and cell death, and deprived the alternations in normal female rats. These changes were restored to normal by estrogen replacement (OVX+E2). These data suggest that β2-AR may be involved in the cardioprotection against ischemic damage, and the cardioprotection may depend on estrogenic environment.
Acknowledgements
This study was supported by the President Support Funding of Xuzhou Medical College (09KJZ31). We gratefully acknowledge the excellent technical assistance of Youjian Qi.
Declaration of interest
The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.