Artículos de revistas
Ventilation Causes Pulmonary Vascular Dilation And Modulates The Nos And Vegf Pathway On Newborn Rats With Cdh
Registro en:
Ventilation Causes Pulmonary Vascular Dilation And Modulates The Nos And Vegf Pathway On Newborn Rats With Cdh. W B Saunders Co-elsevier Inc, v. 50, p. 842-848 MAY-2015.
0022-3468
WOS:000353813300032
10.1016/j.jpedsurg.2014.12.005
Autor
Gallindo
Rodrigo Melo; Lanhellas Goncalves
Frances Lilian; Figueira
Rebeca Lopes; Violin Dias Pereira
Luis Antonio; Bertoncini Simoes
Ana Leda; Schmidt
Augusto Frederico; Sbragia
Lourenco
Institución
Resumen
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Background/Purpose: Congenital diaphragmatic hernia (CDH) is a defect that presents high mortality because of pulmonary hypoplasia and hypertension. Mechanical ventilation changes signaling pathways, such as nitric oxide and VEGF in the pulmonary arterioles. We investigated the production of NOS2 and NOS3 and expression of VEGF and its receptors after ventilation in rat fetuses with CDH. Methods: CDH was induced by Nitrofen. The fetuses were divided into 6 groups: 1) control (C); 2) control ventilated (CV); 3) exposed to nitrofen (N-); 4) exposed to nitrofen ventilated (N-V), 5) CDH and 6) CDH ventilated (CDHV). Fetuses were harvested and ventilated. We assessed body weight (BW), total lung weight (TLW), TLW/BW ratio, the median pulmonary arteriolar wall thickness (MWT). We analyzed the expression of NOS2, NOS3, VEGF and its receptors by immunohistochemistry and Western blotting. Results: BW, TLW, and TLW/BWratiowere greater on C than on N- and CDH (p < 0.05). The MWT was higher in CDH than in CDHV (p < 0.001). CDHV showed increased expression of NOS3 (p < 0.05) and VEGFR1 (p < 0.05), but decreased expression of NOS2 (p < 0.05) and VEGFR2 (p < 0.001) compared to CDH. Conclusion: Ventilation caused pulmonary vasodilation and changed the expression of NOS and VEGF receptors. (C) 2015 Elsevier Inc. All rights reserved. 50 5
842 848 Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) FAPESP [08/50347-9, 11/00794-1, 08/52772-9, 11/12587-0]