Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/47729
Title: Estradiol worsens the syndrome of ischemia-reperfusion injury in an experimental lung transplantation model
Authors: Santana-Rodríguez, Norberto
Clavo, Bernardino 
Llontop, Pedro
López, Ana
García-Castellano, José Manuel
Machín, Rubén P.
Ponce, Miguel A.
Fiuza, María D.
García-Herrera, Ricardo
Brito, Yanira
Yordi, Nagib Atallah
Chirino, Ricardo 
Keywords: Lipid-Peroxidation
17-Beta-Estradiol
Rejection
Melatonin
Estrogen, et al
Issue Date: 2011
Publisher: 0341-2040
Journal: Lung 
Abstract: Ischemia-reperfusion injury (IRI) is a common complication after lung transplantation. There is evidence that reactive oxygen species are involved in its pathogenesis. We designed an experimental study to evaluate whether the administration of antioxidants to lung transplantation recipients protects against IRI and early acute rejection (AR). Twenty-five rats received left lung transplants after 6 h of ischemia. Fifty minutes before the reperfusion, groups of five rats received a single dose of desferrioxamine (20 mg/kg), estradiol (25 mg/kg), or melatonin (10 mg/kg). The animals were killed 48 h after surgery and the postoperative outcome, IRI, and AR were evaluated. The frequency of severe injury and of moderate-to-severe edema was higher in animals treated with estradiol than in the control group (P = 0.022 and P = 0.026, respectively). No significant changes in the degree of IRI or AR were observed in the groups treated with desferrioxamine or melatonin. In our study, treatment with the antioxidants melatonin or desferrioxamine before reperfusion had no effects on IRI damage or on AR frequency or severity. However, treatment with estradiol resulted in a worse postoperative outcome and in severe edema. Therefore, despite the antioxidant capacity of estradiol, it is recommended that an evaluation of these adverse effects of estradiol in human lung transplant recipients be performed.
URI: http://hdl.handle.net/10553/47729
ISSN: 0341-2040
DOI: 10.1007/s00408-011-9287-2
Source: Lung[ISSN 0341-2040],v. 189, p. 251-255
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