Protection from Myocardial Reperfusion Injury by Acute Administration of 17β-Estradiol

Delyani, John A.; Murohara, Toyoaki; Nossuli, Tareck O.; Lefer, Allan M.

doi:10.1006/jmcc.1996.0093

Cited by 63 publications

(30 citation statements)

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“…Cardiac protection by estradiol has been reported in animal models of hemorrhage shock (2,36,42) and ischemic-reperfusion injury (23,67). In this report, we found that an acute postburn administration of estradiol significantly reduced serum troponin I, protected myocardial morphology, and improved cardiac contractility in the burn-injured animals (Fig.…”

Section: Discussionsupporting

confidence: 56%

Estrogen-provided cardiac protection following burn trauma is mediated through a reduction in mitochondria-derived DAMPs

Xiao

Wigginton

Maass

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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Section: Discussionsupporting

confidence: 56%

Estrogen-provided cardiac protection following burn trauma is mediated through a reduction in mitochondria-derived DAMPs

Xiao

Wigginton

Maass

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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“…Indeed, most of the previous studies 19,20 reported a specific postischemic antiinflammatory action on neutrophils after short-term E2 treatment. However, growing evidence suggests that the shortterm effect of E2 could not be predictive of its long-term action.…”

Section: Discussionmentioning

confidence: 99%

Endothelial Estrogen Receptor α Plays an Essential Role in the Coronary and Myocardial Protective Effects of Estradiol in Ischemia/Reperfusion

Favre

Gao

Henry

et al. 2010

ATVB

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Objective-To assess the coronary endothelial protective effects of 17␤-estradiol (E2) and the role of estrogen receptor (ER) ␣ in ischemia/reperfusion (I/R). Methods and Results-E2 exerts protective effects in cardiac I/R. However, the implication in vivo of the endothelium and the cellular targets of the anti-ischemic effects of E2 are unknown. Mice were subjected to I/R (30 minutes of I and 1 hour of R) in vivo, after which acetylcholine-induced relaxation of isolated coronary segments was assessed ex vivo. I/R induced a coronary endothelial dysfunction in untreated ovariectomized mice that was prevented by long-term treatment with E2 in wild-type, but not in ER␣ Ϫ/Ϫ , mice. Chimeric mice inactivated for ER␣ in the hematopoietic compartment remained protected by E2. Further inactivation of endothelial ER␣ abolished the protective action of E2 on coronary endothelial function in Tie2-Cre(ϩ) ER␣ f/f mice. More importantly, E2 significantly limited infarct size in wild-type mice but not in mice deficient in endothelial ER␣, even in the presence of hematopoietic ER␣. Conclusion-Endothelial

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“…Other previous studies have suggested that 17␤-estradiol treatment reduces ischemia/ reperfusion injury. [37][38][39][40][41] Node et al 40 found a reduction of both infarct size and the occurrence of ischemia-and perfusioninduced ventricular arrhythmias and suggested a mediation by NO and the opening of K ca channels in the canine heart. Despite these conflicting observations, it remains unclear which role the respective estrogen receptors per se may play in this process.…”

Section: Mortality Infarct Size and Left Ventricular Remodelingmentioning

confidence: 99%

Female Mice Lacking Estrogen Receptor β Display Prolonged Ventricular Repolarization and Reduced Ventricular Automaticity After Myocardial Infarction

et al. 2005

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Background-Major gender-based differences in the incidence of ventricular tachyarrhythmia after myocardial infarction have been shown in humans. Although the underlying mechanisms are unclear, earlier studies suggest that estrogen receptor-mediated effects play a major role in this process. Methods and Results-We examined the effect of estrogen receptor ␣ (ER␣) and estrogen receptor ␤ (ER␤) on the electrophysiological phenotype in female mice with and without chronic anterior myocardial infarction. There was no significant difference in overall mortality, infarct size, and parameters of left ventricular remodeling when we compared infarcted ER␣-deficient and ER␤-deficient mice with infarcted wild-type animals. In the 12-hour telemetric ECG recording 6 weeks after myocardial infarction, surface ECG parameters did not show significant differences in comparisons of ER␣-deficient mice versus wild-type controls, infarcted versus noninfarcted ER␣-deficient mice, and infarcted ER␣-deficient versus infarcted wild-type mice. However, infarcted ER␤-deficient versus noninfarcted ER␤-deficient mice showed a significant prolongation of the QT (

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Protection from Myocardial Reperfusion Injury by Acute Administration of 17β-Estradiol

Cited by 63 publications

References 1 publication

Estrogen-provided cardiac protection following burn trauma is mediated through a reduction in mitochondria-derived DAMPs

Estrogen-provided cardiac protection following burn trauma is mediated through a reduction in mitochondria-derived DAMPs

Endothelial Estrogen Receptor α Plays an Essential Role in the Coronary and Myocardial Protective Effects of Estradiol in Ischemia/Reperfusion

Female Mice Lacking Estrogen Receptor β Display Prolonged Ventricular Repolarization and Reduced Ventricular Automaticity After Myocardial Infarction

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