Effect of Inhaled Nitric Oxide on Gas Exchange in Patients with Congestive Heart Failure

1999 ◽  
Vol 130 (1) ◽  
pp. 40 ◽  
Author(s):  
Akihiro Matsumoto
The Lancet ◽  
1997 ◽  
Vol 349 (9057) ◽  
pp. 999-1000 ◽  
Author(s):  
Akihiro Matsumoto ◽  
Shin-ichi Momomura ◽  
Yasunobu Hirata ◽  
Teruhiko Aoyagi ◽  
Seiryo Sugiura ◽  
...  

1997 ◽  
Vol 75 ◽  
pp. 120
Author(s):  
Akihiro Matsumoto ◽  
Shin-ichi Momomura ◽  
Yasunobu Hirata ◽  
Seiryo Sugiura ◽  
Masataka Sata ◽  
...  

1998 ◽  
Vol 4 (3) ◽  
pp. 69
Author(s):  
Shunsuke Natori ◽  
Naoyuki Hasebe ◽  
Yin-Tie Jin ◽  
Tomoyuki Matsusaka ◽  
Hideki Nakamura ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Xiaoyu Liu ◽  
John Fassett ◽  
Yidong Wei ◽  
Yingjie Chen

Asymmetric dimethylarginine (ADMA) is an endogenous nitric oxide synthase inhibitor that blocks nitric oxide production, while congestive heart failure is associated with increased plasma and tissue ADMA content. Increased plasma ADMA is a strong and independent predictor of all-cause mortality in the community and the strongest predictor of mortality in patients after myocardial infarction. Recent studies demonstrated that dimethylarginine dimethylaminohydrolase-1 (DDAH1) is the critical enzyme for ADMA degradation and thereby plays an important role in maintaining cardiovascular nitric oxide bioavailability. Interestingly, activation of the farnesoid X receptor (FXR) through the bile acid ursodeoxycholic acid (UDCA) or synthetic FXR agonists, such as GW4064, can increase DDAH1 expression. Thus, modulating DDAH1 activity through FXR receptor agonists such as UDCA could be a therapeutic target for treating reduced nitric oxide bioavailability in congestive heart failure and other cardiovascular diseases.


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