The remodeling of the pulmonary artery in Nitrofen-induced diaphragmatic hernia

Research Project

Project/Area Number	18591951
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Single-year Grants
Section	一般
Research Field	Pediatric surgery
Research Institution	Tokyo Women's Medical University
Principal Investigator	KOUCHI Katsunori Tokyo Women's Medical University, 医学部, 准教授 (40312938)
Co-Investigator(Kenkyū-buntansha)	吉田英生千葉大学, 大学院・医学研究所, 教授 (60210712) 大沼直躬千葉大学, 大学院医学研究院, 教授 (50125910)
Project Period (FY)	2006 – 2009
Project Status	Completed (Fiscal Year 2009)
Budget Amount *help	¥3,710,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥510,000) Fiscal Year 2009: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000) Fiscal Year 2008: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000) Fiscal Year 2007: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000) Fiscal Year 2006: ¥1,500,000 (Direct Cost: ¥1,500,000)
Keywords	胎児 / 横隔膜ヘルニア / 肺高血圧 / VEGF / Endothelin / 胎児治療 / 肺血管増殖因子 / 肺血管抵抗 / VEGR / endothelin
Research Abstract	In Nitrofen-induced congenital diaphragmatic hernia (CDH) fetal rat, the expression of agiopetin-1was low and the ET1, ET1 recepter A/B was high. The other genes ; VEGF、angiopoietin-2、ephrinA1,B2、PDGFb and their receptor was no alternation compared with normal fetal rat. This suggested that over expression of ET1 and its receptor A/B induced the wall thickness of CDH fetal rat. Therefore, We examined the effect of ET receptor antagonist to feta dam. Pregnant rat gavaged ET1 antagonist. In these dam, the thickness of the pulmonary artery was not observed and the expression of VEGF was increased. In the other gene expression were not altered. In conclusion : ET receptor antagonist increased the expression of VEGF and reduced the wall thickness of the pulmonary artery in CDH dam. We supposed the high expression of VEGF made the prevention of the wall thickness. ET receptor antagonist has effect to prevent the pulmonary hypertension in newborn CDH.