Thrombopoietin inside the pulmonary vessels in patients with and without pulmonary hypertension.

There is substantial evidence that platelet production and release take place in the lungs. Thrombopoietin (Tpo) stimulation can cause platelet release in the pulmonary vasculature. On the other hand, myelofibrosis can occur in Tpo-overexpressing transgenic mice models, and there is unexplained pulmonary hypertension in chronic myeloproliferative disorders including primary myelofibrosis. In this study, we aimed to assess local Tpo concentrations inside the pulmonary artery and associated vessels in humans. We measured Tpo concentrations in plasma samples taken concurrently from the right ventricle, the pulmonary artery, and the left ventricle during cardiac catheterization in patients with and without pulmonary hypertension. The study group comprised 10 patients with normal pulmonary arterial pressure (Group A, male/female 4/6, mean age 48 +/- 19) and 14 patients with pulmonary hypertension (Group B, male/female 9/5, mean age 57 +/- 16). The Tpo levels inside the right ventricle, the pulmonary artery and the left ventricle were 33.3 +/- 15.6, 47.2 +/- 33.9, and 34.4 +/- 18.6 pg/ml, respectively, in Group A; and 85.0 +/- 39.8, 128.4 +/- 50.4, and 81.5 +/- 35.5 pg/ml, respectively, in Group B. Levels of the Tpo were significantly higher in all three localizations in Group B compared to Group A. Moreover, the Tpo concentration inside the pulmonary artery is significantly higher than the Tpo concentrations in the right and left ventricles in Group B patients. There were positive correlations between the Tpo levels and pulmonary artery systolic pressure over the whole patient group. In conclusion, there could be an association between pulmonary hypertension and Tpo level. Moreover, lung vasculature holding the major regulatory thrombopoietic hormone, Tpo, may be an important place for megakaryocytopoiesis.