Postischemic Infusion of 17-β-Estradiol Protects Myocardial Function and Viability

Andrew M. Terrell, Paul R. Crisostomo, Troy A. Markel, Meijing Wang, Aaron M. Abarbanell, Jeremy L. Herrmann, Daniel R. Meldrum

Research output: Contribution to journalArticle

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Abstract

Background: Females demonstrate improved cardiac recovery after ischemia/reperfusion injury compared with males. Attenuation of myocardial dysfunction with preischemic estradiol suggests that estrogen may be an important mediator of this cardioprotection. However, it remains unclear whether post-injury estradiol may have clinical potential in the treatment of acute myocardial infarction. We hypothesize that postischemic administration of 17β-estradiol will decrease myocardial ischemia/reperfusion injury and improve left ventricular cardiac function. Materials and methods: Adult male Sprague Dawley rat hearts (n = 20) (Harlan, Indianapolis, IN) were isolated, perfused with Krebs-Henseleit solution via Langendorff model, and subjected to 15 min of equilibration, 25 min of warm ischemia, and 40 min reperfusion. Experimental hearts received postischemic 17β-estradiol infusion, 1 nm (n = 4), 10 nm (n = 4), 25 nm (n = 4), or 50 nm (n = 4), throughout reperfusion. Control hearts (n = 4) were infused with perfusate vehicle. Results: Postischemic recovery of left ventricular developed pressure was significantly greater with 1 nm (51.6% ± 7.4%) and 10 nm estradiol (47.7% ± 8.6%) than with vehicle (37.8% ± 9.7%) at end reperfusion. There was also greater recovery of the end diastolic pressure with 1 nm (47.8 ± 4.0 mmHg) and 10 nm estradiol (54.0 ± 4.0) compared with vehicle (75.3 ± 7.5). Further, 1 nm and 10 nm estrogen preserved coronary flow after ischemia and decreased coronary effluent lactated dehydrogenase compared with controls. Estrogen at 25 nm and 50 nm did not provide additional benefit in terms of functional recovery. Estrogen at all concentrations increased extracellular signal-regulated protein kinase phosphorylation. Conclusions: Postischemic infusion of 17β-estradiol protects myocardial function and viability. The attractive potential for the clinical application of postischemic estrogen therapy warrants further study to elucidate the mechanistic pathways and differences between males and females.

Original languageEnglish
Pages (from-to)218-224
Number of pages7
JournalJournal of Surgical Research
Volume146
Issue number2
DOIs
StatePublished - May 15 2008

Fingerprint

Estradiol
Estrogens
Reperfusion
Reperfusion Injury
Myocardial Reperfusion Injury
Warm Ischemia
Extracellular Signal-Regulated MAP Kinases
Ventricular Pressure
Left Ventricular Function
Protein Kinases
Myocardial Ischemia
Sprague Dawley Rats
Oxidoreductases
Ischemia
Myocardial Infarction
Phosphorylation
Blood Pressure
Wounds and Injuries

Keywords

  • estrogen
  • myocardial infarction
  • recovery
  • sex hormones

ASJC Scopus subject areas

  • Surgery

Cite this

Terrell, A. M., Crisostomo, P. R., Markel, T. A., Wang, M., Abarbanell, A. M., Herrmann, J. L., & Meldrum, D. R. (2008). Postischemic Infusion of 17-β-Estradiol Protects Myocardial Function and Viability. Journal of Surgical Research, 146(2), 218-224. https://doi.org/10.1016/j.jss.2007.05.021

Postischemic Infusion of 17-β-Estradiol Protects Myocardial Function and Viability. / Terrell, Andrew M.; Crisostomo, Paul R.; Markel, Troy A.; Wang, Meijing; Abarbanell, Aaron M.; Herrmann, Jeremy L.; Meldrum, Daniel R.

In: Journal of Surgical Research, Vol. 146, No. 2, 15.05.2008, p. 218-224.

Research output: Contribution to journalArticle

Terrell, AM, Crisostomo, PR, Markel, TA, Wang, M, Abarbanell, AM, Herrmann, JL & Meldrum, DR 2008, 'Postischemic Infusion of 17-β-Estradiol Protects Myocardial Function and Viability', Journal of Surgical Research, vol. 146, no. 2, pp. 218-224. https://doi.org/10.1016/j.jss.2007.05.021
Terrell, Andrew M. ; Crisostomo, Paul R. ; Markel, Troy A. ; Wang, Meijing ; Abarbanell, Aaron M. ; Herrmann, Jeremy L. ; Meldrum, Daniel R. / Postischemic Infusion of 17-β-Estradiol Protects Myocardial Function and Viability. In: Journal of Surgical Research. 2008 ; Vol. 146, No. 2. pp. 218-224.
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abstract = "Background: Females demonstrate improved cardiac recovery after ischemia/reperfusion injury compared with males. Attenuation of myocardial dysfunction with preischemic estradiol suggests that estrogen may be an important mediator of this cardioprotection. However, it remains unclear whether post-injury estradiol may have clinical potential in the treatment of acute myocardial infarction. We hypothesize that postischemic administration of 17β-estradiol will decrease myocardial ischemia/reperfusion injury and improve left ventricular cardiac function. Materials and methods: Adult male Sprague Dawley rat hearts (n = 20) (Harlan, Indianapolis, IN) were isolated, perfused with Krebs-Henseleit solution via Langendorff model, and subjected to 15 min of equilibration, 25 min of warm ischemia, and 40 min reperfusion. Experimental hearts received postischemic 17β-estradiol infusion, 1 nm (n = 4), 10 nm (n = 4), 25 nm (n = 4), or 50 nm (n = 4), throughout reperfusion. Control hearts (n = 4) were infused with perfusate vehicle. Results: Postischemic recovery of left ventricular developed pressure was significantly greater with 1 nm (51.6{\%} ± 7.4{\%}) and 10 nm estradiol (47.7{\%} ± 8.6{\%}) than with vehicle (37.8{\%} ± 9.7{\%}) at end reperfusion. There was also greater recovery of the end diastolic pressure with 1 nm (47.8 ± 4.0 mmHg) and 10 nm estradiol (54.0 ± 4.0) compared with vehicle (75.3 ± 7.5). Further, 1 nm and 10 nm estrogen preserved coronary flow after ischemia and decreased coronary effluent lactated dehydrogenase compared with controls. Estrogen at 25 nm and 50 nm did not provide additional benefit in terms of functional recovery. Estrogen at all concentrations increased extracellular signal-regulated protein kinase phosphorylation. Conclusions: Postischemic infusion of 17β-estradiol protects myocardial function and viability. The attractive potential for the clinical application of postischemic estrogen therapy warrants further study to elucidate the mechanistic pathways and differences between males and females.",
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