Continuous infusion of epoprostenol improves the net balance between pulmonary endothelin-1 clearance and release in primary pulmonary hypertension.
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B. Groves | D. Stewart | R. Barst | D. Badesch | V. Tapson | S. Murali | D. Langleben | R. Bourge | J. Crow | L. Clayton | E. Shalit | N. Ettinger | W. Long | M. Jöbsis | S. Blackburn | R. Barst
[1] D. Badesch,et al. Prostacyclin synthase expression is decreased in lungs from patients with severe pulmonary hypertension. , 1999, American journal of respiratory and critical care medicine.
[2] K. Shroyer,et al. Monoclonal endothelial cell proliferation is present in primary but not secondary pulmonary hypertension. , 1998, The Journal of clinical investigation.
[3] S. Rich,et al. Reduction in pulmonary vascular resistance with long-term epoprostenol (prostacyclin) therapy in primary pulmonary hypertension. , 1998, The New England journal of medicine.
[4] R. Barst,et al. Continuous infusion of prostacyclin normalizes plasma markers of endothelial cell injury and platelet aggregation in primary pulmonary hypertension. , 1997, Circulation.
[5] J. Dupuis,et al. The orally active ET(A) receptor antagonist (+)-(S)-2-(4,6-dimethoxy-pyrimidin-2-yloxy)-3-methoxy-3,3-diphe nyl-propionic acid (LU 135252) prevents the development of pulmonary hypertension and endothelial metabolic dysfunction in monocrotaline-treated rats. , 1997, The Journal of pharmacology and experimental therapeutics.
[6] B. Brundage,et al. Primary pulmonary hypertension: improved long-term effects and survival with continuous intravenous epoprostenol infusion. , 1997, Journal of the American College of Cardiology.
[7] G. Koch,et al. Effects of Long-term Infusion of Prostacyclin (Epoprostenol) on Echocardiographic Measures of Right Ventricular Structure and Function in Primary Pulmonary Hypertension , 1997 .
[8] D. Stewart,et al. Human pulmonary circulation is an important site for both clearance and production of endothelin-1. , 1996, Circulation.
[9] T. Rubin,et al. PGE2 and PGI2 inhibit ET-1 secretion from endothelial cells by stimulating particulate guanylate cyclase. , 1996, The American journal of physiology.
[10] C. Goresky,et al. Pulmonary clearance of circulating endothelin-1 in dogs in vivo: exclusive role of ETB receptors. , 1996, Journal of applied physiology.
[11] B. Groves,et al. A comparison of continuous intravenous epoprostenol (prostacyclin) with conventional therapy for primary pulmonary hypertension. , 1996, The New England journal of medicine.
[12] R. Johns,et al. Endothelial nitric oxide synthase in the lungs of patients with pulmonary hypertension. , 1995, The New England journal of medicine.
[13] T. Ogihara,et al. Overexpression of prostacyclin synthase inhibits growth of vascular smooth muscle cells. , 1995, Biochemical and biophysical research communications.
[14] A Giaid,et al. Reduced expression of endothelial nitric oxide synthase in the lungs of patients with pulmonary hypertension. , 1995, The New England journal of medicine.
[15] S. Ishikawa,et al. Elevated levels of plasma endothelin-1 in young patients with pulmonary hypertension caused by congenital heart disease are decreased after successful surgical repair. , 1995, The Journal of thoracic and cardiovascular surgery.
[16] G. Simonneau,et al. Continuous Infusion of Prostacyclin Decreases Plasma Levels of t-PA and PAI-1 in Primary Pulmonary Hypertension , 1995, Thrombosis and Haemostasis.
[17] E. Levin,et al. Prostaglandin E2 and prostacyclin inhibit the production and secretion of endothelin from cultured endothelial cells. , 1994, The Journal of biological chemistry.
[18] D. Laporta,et al. Endothelin-1 in acute lung injury and the adult respiratory distress syndrome. , 1993, The American review of respiratory disease.
[19] V. Fuster,et al. Prostacyclin (epoprostenol) and heart-lung transplantation as treatments for severe pulmonary hypertension. , 1993, British heart journal.
[20] D. Stewart,et al. Expression of endothelin-1 in the lungs of patients with pulmonary hypertension. , 1993, The New England journal of medicine.
[21] B. Groves,et al. An imbalance between the excretion of thromboxane and prostacyclin metabolites in pulmonary hypertension. , 1992, The New England journal of medicine.
[22] P. Binkley,et al. Plasma Endothelin Correlates With the Extent of Pulmonary Hypertension in Patients With Chronic Congestive Heart Failure , 1992, Circulation.
[23] D. Faller,et al. Hypoxia induces endothelin gene expression and secretion in cultured human endothelium. , 1991, The Journal of clinical investigation.
[24] D. Stewart,et al. Increased plasma endothelin-1 in pulmonary hypertension: marker or mediator of disease? , 1991, Annals of internal medicine.
[25] D. Stewart,et al. Immunoreactive endothelin in human plasma: marked elevations in patients in cardiogenic shock. , 1989, Biochemical and biophysical research communications.
[26] J. Vane,et al. Pressor effects of circulating endothelin are limited by its removal in the pulmonary circulation and by the release of prostacyclin and endothelium-derived relaxing factor. , 1988, Proceedings of the National Academy of Sciences of the United States of America.
[27] L. Rubin,et al. Primary pulmonary hypertension. , 1997, The New England journal of medicine.
[28] Sadao Kimura,et al. A novel potent vasoconstrictor peptide produced by vascular endothelial cells , 1988, Nature.
[29] E H Bergofsky,et al. Primary pulmonary hypertension. A national prospective study. , 1987, Annals of internal medicine.
[30] G. W. Snedecor. STATISTICAL METHODS , 1967 .
[31] Inda,et al. A COMPARISON OF CONTINUOUS INTRAVENOUS EPOPROSTENOL ( PROSTACYCLIN ) WITH CONVENTIONAL THERAPY FOR PRIMARY PULMONARY HYPERTENSION , 2000 .
[32] S. Oparil,et al. Endothelin-A receptor antagonist prevents acute hypoxia-induced pulmonary hypertension in the rat. , 1995, The American journal of physiology.