Fibrosis of pulmonary vascular remodeling in carotid artery-jugular vein shunt pulmonary artery hypertension model of rats

Eur J Cardiothorac Surg. 2012 Jan;41(1):162-6. doi: 10.1016/j.ejcts.2011.04.031.

Abstract

Objective: The aim of the present study was to observe the changes of hemodynamics, stereology in pulmonary vascular remodeling and messenger RNA (mRNA) expressions of transforming growth factor beta 1, and receptors in carotid artery-jugular vein (CA-JV) shunt pulmonary artery hypertension model of rats.

Methods: Thirty-six Sprague-Dawley rats were randomized into three groups: CA-JV group, monocrotaline (MCT) administration group, and control group. Left CA-JV shunts were established in CA-JV group. Dorsal subcutaneous injections of MCT (60 mg kg(-1)) were received in MCT group. Ligations of left common carotid artery and external jugular vein were performed in control group. Right ventricular systolic pressure (RVSP) measurement, histological evaluation of the pulmonary tissue, and mRNA levels of transforming growth factor beta 1 (TGFß1), receptor 1 and receptor 2, were investigated after 6 weeks on MCT group, and after 12 weeks on both control and CA-JV groups.

Results: Compared with control group, RVSP, percentage of fibrous tissue (F%) in pulmonary arterioles, mRNA levels of TGFß1, and receptors of CA-JVand MCT groups increased significantly. Severe hemodynamics change was found in MCT groups. On the other hand, CA-JV group demonstrated more obvious fibrogenesis and TGFß1 signals' upregulation in two pulmonary artery hypertension (PAH) models.

Conclusions: CA-JV shunt model of rats was a well-established PAH animal model simulating congenital heart disease with systemic-pulmonary shunt.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Arterioles / pathology
  • Arteriovenous Shunt, Surgical / methods
  • Carotid Artery, Common / surgery
  • Disease Models, Animal*
  • Fibrosis
  • Gene Expression Regulation / physiology
  • Hemodynamics / physiology
  • Hypertension, Pulmonary / etiology*
  • Hypertension, Pulmonary / metabolism
  • Hypertension, Pulmonary / pathology
  • Hypertension, Pulmonary / physiopathology
  • Jugular Veins / surgery
  • Male
  • Pulmonary Artery / pathology*
  • RNA, Messenger / genetics
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Transforming Growth Factor beta / biosynthesis
  • Receptors, Transforming Growth Factor beta / genetics
  • Transforming Growth Factor beta1 / biosynthesis
  • Transforming Growth Factor beta1 / genetics

Substances

  • RNA, Messenger
  • Receptors, Transforming Growth Factor beta
  • Transforming Growth Factor beta1