| Grant number: | 11/00794-1 |
| Support Opportunities: | Regular Research Grants |
| Start date: | May 01, 2011 |
| End date: | October 31, 2013 |
| Field of knowledge: | Health Sciences - Medicine - Surgery |
| Principal Investigator: | Lourenço Sbragia Neto |
| Grantee: | Lourenço Sbragia Neto |
| Host Institution: | Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil |
Abstract
Congenital Diaphragmatic Hernia (CDH) is a defect in the formation of the diaphragm muscle that affects approximately 1:2500 live births and has high rates of fetal and neonatal mortality due to pulmonary hypoplasia and hypertension. Histologically in the lungs of CDH both the alveolar and vasculature are altered which ends up causing difficulty in ventilation of the baby at birth. This defect can be obtained experimentally by ingestion of nitrofen in rats via gavage at 9.5 days of gestation resulting in 30% of affected fetuses with CDH. Tracheal occlusion (TO) stimulates the growth and fetal lung maturation and reduces the impedance to blood flow in sheep with CDH, suggesting a reversal in pulmonary hypertension secondary to the defect. The vascular changes that occur in the HDC and that possibly are reversed by TO relates to the phenomenon of angiogenesis, which in turn is regulated by factors and their receptors by still unknown mechanisms that involve the production of nitric oxide (NO) and its synthases (NOS) associated with vascular growth. Recently with the aid FAPESP project, we found that the TO associated with intra-tracheal albumin can increase the density of cell proliferation and 45 associated with steroid TO restored the expression of VEGF receptors in experimental CDH, however, these studies did not aim nether to evaluate the route of NO nor the in vivo vascular response after birth. So evaluate the relationship between the experimental treatment of CDH with the production of nitric oxide by the isoforms, especially eNOS and its interaction with TO on the fetal development of pulmonary vasculature, especially on the VEGF receptors may provide subsidies for understanding the pathophysiology and treatment of disease. (AU)
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