Fetal pulmonary vascular remodeling in a rat model induced by hypoxia and indomethacin

J Matern Fetal Neonatal Med. 2011 Jan;24(1):172-82. doi: 10.3109/14767058.2010.482608. Epub 2010 May 12.

Abstract

Objective: This study sought to determine the effect of combined treatment of hypoxia plus indomethacin on pulmonary vascular remodeling in fetal rats.

Methods: Hypoxia and indomethacin were used to treat pregnant rats during 19-21 days of gestation. The adventitia, media, and intima of pulmonary arteries from fetal rats were assessed. Western blots were used for determining the abundance of smooth muscle specific alpha-actin protein (α-SMA), elastin, and endothelial nitric oxide synthase (eNOS) in lung tissues. Plasma brain-type natriuretic peptide (BNP) levels, reflecting the increased right ventricular load or pulmonary arterial pressure, were detected.

Results: The ratio of left ventricular free wall plus septum to right ventricular weight significantly increased in hypoxia plus indomethacin-treated group. The medial thickness percentage of pulmonary arteries of < 100 μm and ≥100 μm in diameter from hypoxia plus indomethacin-treated group was higher than that from control or single treatment group. Vascular elastin area percentage and immunostaining density of eNOS from the combined-treated group were higher than other groups. The relative abundance of α-SMA, elastin, and eNOS and plasma BNP levels in hypoxia plus indomethacin-treated group also significantly increased compared with other groups.

Conclusions: Hypoxia and indomethacin had synergistic effect on fetal pulmonary vascular remodeling. This rat model induced by combined treatments can mimic human persistent pulmonary hypertension of the newborn.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Animals
  • Animals, Newborn
  • Blotting, Western
  • Cardiovascular Agents
  • Disease Models, Animal
  • Elastin / metabolism
  • Female
  • Humans
  • Hypoxia / complications
  • Indomethacin
  • Infant, Newborn
  • Lung / blood supply
  • Lung / metabolism
  • Myocardium / pathology*
  • Natriuretic Peptide, Brain / blood*
  • Nitric Oxide Synthase Type III / metabolism
  • Persistent Fetal Circulation Syndrome / blood
  • Persistent Fetal Circulation Syndrome / chemically induced
  • Persistent Fetal Circulation Syndrome / pathology*
  • Pulmonary Artery / ultrastructure*
  • Rats
  • Rats, Sprague-Dawley

Substances

  • Actins
  • Cardiovascular Agents
  • natriuretic peptide precursor type B, rat
  • smooth muscle actin, rat
  • Natriuretic Peptide, Brain
  • Elastin
  • Nitric Oxide Synthase Type III
  • Nos3 protein, rat
  • Indomethacin