HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

Susceptibility to cardiac ischemia/reperfusion injury is modulated by chronic estrogen status.

Abstract
The purpose of this study was to test whether the susceptibility of the heart to ischemia/reperfusion injury is modulated by the chronic estrogen status, i.e., increased with estrogen deficiency and attenuated by pharmacologic estrogen supplementation. In addition, the study tested whether estrogen-dependent changes in mechanical function are associated with alterations of cardiac high-energy phosphate metabolism. Rats were ovariectomized, not ovariectomized, or ovariectomized and treated with subcutaneous estrogen pellets (1.5 mg/21 d) (n = 8-11 per group). Three weeks later, hearts were isolated and perfused isovolumically under constant perfusion pressure conditions. Hearts were subjected to 15 min of total global ischemia (37 degrees C) and 30 min of reperfusion. Simultaneous [31P] nuclear magnetic resonance spectra were recorded throughout this protocol to monitor changes in ATP, phosphocreatine, and inorganic phosphate content. Whereas preischemic values for heart rate, end-diastolic pressure, and coronary flow were not different among groups, left ventricular developed pressure was slightly but significantly decreased in the estrogen-treated group (p < 0.05). However, treated hearts showed improved recovery of left ventricular developed pressure on reperfusion (89 +/- 4% in control rats, 70 +/- 8% in ovariectomized hearts, and 114 +/- 9% of preischemic values in estrogen-treated rats). However, changes in ATP, phosphocreatine, and inorganic phosphate during ischemia were as previously described and were unaffected by chronic estrogen status. In conclusion, in the isolated buffer-perfused rat heart, estradiol treatment caused improved functional recovery after ischemia/reperfusion injury. This improvement, however, did not include preservation of high-energy phosphate metabolism. Other potential mechanisms include an anti-oxidant activity of 17beta-estradiol-and estrogen-induced alterations in glucose metabolism.
AuthorsStephanie Beer, Martin Reincke, Maike Kral, Su Zan Lie, Sonja Steinhauer, Harald H H W Schmidt, Bruno Allolio, Stefan Neubauer
JournalJournal of cardiovascular pharmacology (J Cardiovasc Pharmacol) Vol. 40 Issue 3 Pg. 420-8 (Sep 2002) ISSN: 0160-2446 [Print] United States
PMID12198328 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Estrogens
  • Estradiol
Topics
  • Animals
  • Disease Susceptibility (blood, metabolism)
  • Estradiol (pharmacology, therapeutic use)
  • Estrogens (blood, metabolism)
  • Female
  • Hemodynamics (drug effects, physiology)
  • Myocardial Ischemia (blood, drug therapy, metabolism)
  • Myocardial Reperfusion Injury (blood, drug therapy, metabolism)
  • Ovariectomy
  • Rats
  • Rats, Wistar

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: