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Title: 17 beta-Estradiol protects against lung injuries after brain death in male rats
Authors: VIEIRA, Roberta FigueiredoBREITHAUPT-FALOPPA, Ana CristinaMATSUBARA, Bruno CarvalhoRODRIGUES, GeovanaSANCHES, Marcelo PetrofARMSTRONG- JR., RobertoFERREIRA, Sueli GomesCORREIA, Cristiano de JesusMOREIRA, Luiz Felipe P.SANNOMIYA, Paulina
Citation: JOURNAL OF HEART AND LUNG TRANSPLANTATION, v.37, n.11, p.1381-1387, 2018
Abstract: BACKGROUND: Brain death elicits microvascular dysfunction and inflammation, and thereby compromises lung viability for transplantation. As 17 beta-estradiol was shown to be anti-inflammatory and vascular protective, we investigated its effects on lung injury after brain death in male rats. METHODS: Wistar rats were assigned to: sham-operation by trepanation only (SH, n = 7); brain death (BD, n = 7); administration of 17-estradiol (280 tg/kg, iv) at 60 minutes after brain death (BD-E2, n = 7). Experiments were performed 180 minutes thereafter. Histopathological changes in the lung were evaluated by histomorphometry. Gene expression of inducible nitric oxide synthase (iNOS), endothelial nitric oxide synthase (eNOS), and endothelin-1 was measured by real-time polymerise chain reaction. Protein expression of NO synthases, endothelin-1, platelet endothelial cell adhesion molecule-1 (PECAM-1), vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), BCL-2, and caspase 3 was assessed by immunohistochemistry. Cytokines were quantified by enzyme linked immunosorbent assay. RESULTS: Treatment with 17P-estradiol after brain death decreased lung edema and hemorrhage (p < 0.0001), and serum levels of cytokine-induced neutrophil chemoattractant-1 (CINC-1; p = 0.0020). iNOS (p < 0.0001) and VCAM-1 (p < 0.0001) also diminished at protein levels, while eNOS accumulated (p = 0.0002). However, gene expression of iNOS, eNOS, and endothelin-1 was comparable among groups, as was protein expression of endothelin-1, ICAM-1, BCL-2, and caspase 3. CONCLUSIONS: 17P-Estradiol effectively reduces lung injury in brain-dead rats mainly due to its ability to regulate NO synthases. Thus, the drug may improve lung viability for transplantation. J Heart Lung Transplant 2018;37:1381-1387 (C) 2018 International Society for Heart and Lung Transplantation. All rights reserved.
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Artigos e Materiais de Revistas Científicas - FM/MCP
Departamento de Cardio-Pneumologia - FM/MCP

Artigos e Materiais de Revistas Científicas - HC/ICHC
Instituto Central - HC/ICHC

Artigos e Materiais de Revistas Científicas - HC/InCor
Instituto do Coração - HC/InCor

Artigos e Materiais de Revistas Científicas - LIM/11
LIM/11 - Laboratório de Cirurgia Cardiovascular e Fisiopatologia da Circulação

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