Abstract
Rationale: About 30-40% of patients of idiopathic pulmonary arterial hypertension (IPAH) have thyroid dysfunction, in particular hypothyroidism. Pulmonary vascular remodeling in PAH is characterized by proliferation of vascular cells and thyroid hormones are known to promote angiogenesis (Mousa et al J Cardiovasc Pharmacol, 2005). We therefore hypothesized that hypothyroidism would improve pulmonary vascular remodeling in a model of angioproliferative pulmonary hypertension (SuHx model).
Objectives: To clarify the effect of thyroid hormone on pulmonary vascular remodeling in SuHx treated rats.
Methods: PAH was induced by the combined exposure of rats to the VEGF receptor blocker SU5416 and hypoxia (SuHx). Hypothyroidism was induced by PTU (10mg/kg, 5times a week), two weeks after the initial SU5416 dose (SuHx) rats. RV function was determined by echocardiography. Right ventricular pressure was measured by direct insertion of a conductance catheter into the heart.
Results: In SuHx rats, pulmonary vascular remodeling and pulmonary hypertension were decreased after PTU treatment and completely suppressed after thyroidectomy.
Conclusions: Thyroid dysfunction may affect the progression of pulmonary vascular cell proliferation in patients with PAH.
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