ID | 55318 |
FullText URL | |
Author |
Saito, Yukihiro
Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Nakamura, Kazufumi
Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Akagi, Satoshi
Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Sarashina, Toshihiro
Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Ejiri, Kentaro
Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Miura, Aya
Division of Cardiology, National Hospital Organization Okayama Medical Center
Ogawa, Aiko
Division of Cardiology, National Hospital Organization Okayama Medical Center
Matsubara, Hiromi
Division of Cardiology, National Hospital Organization Okayama Medical Center
Ito, Hiroshi
Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
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Abstract | The release of endogenous prostacyclin (PGI2) is depressed in patients with pulmonary arterial hypertension (PAH). PGI2 replacement therapy by epoprostenol infusion is one of the best treatments available for PAH. Here, we provide an overview of the current clinical data for epoprostenol. Epoprostenol treatment improves symptoms, exercise capacity, and hemodynamics, and is the only treatment that has been shown to reduce mortality in patients with idiopathic PAH (IPAH) in randomized clinical trials. We have reported that high-dose epoprostenol therapy (>40 ng/kg/min) also results in marked hemodynamic improvement in some patients with IPAH. High-dose epoprostenol has a pro-apoptotic effect on PAH-PASMCs via the IP receptor and upregulation of Fas ligand (FasL) in vitro. However, long-term intravenous administration of epoprostenol is sometimes associated with catheter-related infections and leads to considerable inconvenience for the patient. In the future, the development of new routes of administration or the development of powerful PGI2 analogs, IP-receptor agonists, and gene and cell-based therapy enhancing PGI2 production with new routes of administration is required.
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Keywords | apoptosis
prostacyclin
pulmonary arterial hypertension
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Note | 学位審査副論文
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Published Date | 2015-05-14
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Publication Title |
Vascular Health and Risk Management
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Volume | volume11
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Publisher | Dove Medical Press
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Start Page | 265
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End Page | 270
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ISSN | 1176-6344
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NCID | AA12158664
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Content Type |
Journal Article
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language |
English
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OAI-PMH Set |
岡山大学
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Copyright Holders | https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja
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File Version | publisher
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PubMed ID | |
DOI | |
Web of Science KeyUT | |
Related Url | https://doi.org/10.2147/VHRM.S50368
http://ousar.lib.okayama-u.ac.jp/55246
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