Thromboxane synthetase inhibition in primary pulmonary hypertension

Chest. 1987 Mar;91(3):356-60. doi: 10.1378/chest.91.3.356.


Thromboxane synthetase inhibitors have been shown to reduce thromboxane, a potent vasoconstrictor, and increase prostacyclin, a potent vasodilator, in normal subjects. We evaluated the acute and chronic (three months) effects of the thromboxane synthetase inhibitor CGS13080 administered 200 mg every six hours on the resting hemodynamics in ten patients with primary pulmonary hypertension (PPH), and on their response to 20 mg of nifedipine given sublingually before and after the thromboxane synthetase inhibitor treatment. It was concluded that one can modulate the levels of endogenous thromboxane and prostacyclin in patients with primary pulmonary hypertension using a thromboxane synthetase inhibitor. Although the thromboxane synthetase inhibitor alone produced only modest hemodynamic changes over time, the addition of nifedipine was able to produce a further lowering of pulmonary artery pressure and pulmonary vascular resistance.

MeSH terms

  • Adult
  • Epoprostenol / metabolism
  • Female
  • Humans
  • Hypertension, Pulmonary / drug therapy*
  • Imidazoles / pharmacology
  • Imidazoles / therapeutic use*
  • Male
  • Middle Aged
  • Nifedipine / therapeutic use
  • Pyridines / pharmacology
  • Pyridines / therapeutic use*
  • Thromboxane B2 / metabolism
  • Thromboxane-A Synthase / antagonists & inhibitors*


  • Imidazoles
  • Pyridines
  • Thromboxane B2
  • pirmagrel
  • Epoprostenol
  • Thromboxane-A Synthase
  • Nifedipine