Endothelin A receptor blockade improves regression of flow-induced pulmonary vasculopathy in piglets

J Thorac Cardiovasc Surg. 2010 Sep;140(3):677-83. doi: 10.1016/j.jtcvs.2010.01.004.

Abstract

Objectives: In patients with chronic thromboembolic pulmonary hypertension, high flow in unobstructed lung regions may induce small-vessel damage responsible for persistent pulmonary hypertension after pulmonary thromboendarterectomy. In piglets, closure of an experimental aortopulmonary shunt reverses the flow-induced vascular lesions and diminishes the elevated levels of messenger RNA (mRNA) expression for endothelin-1 and endothelin receptor A (ETA). We wanted to study the effect of the ETA antagonist TBC 3711 on reversal of flow-induced pulmonary vascular lesions.

Methods: Twenty piglets were studied. In 15 piglets, pulmonary vasculopathy was induced by creating an aortopulmonary shunt. After 5 weeks of shunting, some animals were studied (n = 5); others underwent shunt closure for 1 week with (n = 5) or without (n = 5) TBC3711 treatment. Anti-ETA treatment started 1 week before and ended 1 week after the shunt closure. The controls were sham-operated animals (n = 5).

Results: High blood flow led to medial hypertrophy of the distal pulmonary arteries (54.9% +/- 1.3% vs 35.3% +/- 0.9%; P < .0001) by stimulating smooth muscle cell proliferation (proliferating cell nuclear antigen) and increased the expression of endothelin-1, ETA or endothelin receptor type A or endothelin receptor A, angiopoietin 1, and Tie2 (real-time polymerase chain reaction). One week after shunt closure, gene expression levels were normal and smooth muscle cells showed increased apoptosis (terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling) without proliferation. However, pulmonary artery wall thickness returned to control values only in the group given TBC3711 (33.2% +/- 8% with and 50.3% +/- 1.3% without; P < .05).

Conclusions: Anti-ETA therapy accelerated the reversal of flow-induced pulmonary arterial disease after flow correction. In patients with chronic thromboembolic pulmonary hypertension and severe distal pulmonary vasculopathy, anti-ETA agents may prove useful for preventing persistent pulmonary hypertension after pulmonary thromboendarterectomy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiopoietin-1 / genetics
  • Animals
  • Animals, Newborn
  • Antihypertensive Agents / pharmacology*
  • Aorta / physiopathology
  • Aorta / surgery
  • Apoptosis / drug effects
  • Cell Proliferation
  • Disease Models, Animal
  • Endothelin A Receptor Antagonists*
  • Endothelin-1 / genetics
  • Endothelin-1 / metabolism
  • Gene Expression Regulation / drug effects
  • Hemodynamics / drug effects
  • Hypertension, Pulmonary / drug therapy*
  • Hypertension, Pulmonary / metabolism
  • Hypertension, Pulmonary / pathology
  • Hypertension, Pulmonary / physiopathology
  • Hypertrophy
  • Isoxazoles / pharmacology*
  • Muscle, Smooth, Vascular / drug effects
  • Muscle, Smooth, Vascular / metabolism
  • Muscle, Smooth, Vascular / physiopathology
  • Pulmonary Artery / drug effects*
  • Pulmonary Artery / metabolism
  • Pulmonary Artery / pathology
  • Pulmonary Artery / physiopathology
  • Pulmonary Artery / surgery
  • Pulmonary Circulation / drug effects*
  • Pulmonary Embolism / drug therapy*
  • Pulmonary Embolism / metabolism
  • Pulmonary Embolism / pathology
  • Pulmonary Embolism / physiopathology
  • RNA, Messenger / metabolism
  • Receptor, Endothelin A / genetics
  • Receptor, Endothelin A / metabolism
  • Receptor, TIE-2 / genetics
  • Sulfones / pharmacology*
  • Swine
  • Time Factors

Substances

  • Angiopoietin-1
  • Antihypertensive Agents
  • Endothelin A Receptor Antagonists
  • Endothelin-1
  • Isoxazoles
  • N-(2-acetyl-4,6-dimethylphenyl)-3-(3,4-dimethylisoxazol-5-ylsulfamoyl)thiophene-2-carboxamide
  • RNA, Messenger
  • Receptor, Endothelin A
  • Sulfones
  • Receptor, TIE-2