Long-term administration of tolvaptan increases myocardial remodeling and mortality via exacerbation of congestion in mice heart failure model after myocardial infarction

2016 ◽  
Vol 221 ◽  
pp. 302-309 ◽  
Author(s):  
Akiyo Eguchi ◽  
Toshihiro Iwasaku ◽  
Yoshitaka Okuhara ◽  
Yoshiro Naito ◽  
Toshiaki Mano ◽  
...  
2006 ◽  
Vol 132 (4) ◽  
pp. 918-924 ◽  
Author(s):  
Hiroki Hata ◽  
Goro Matsumiya ◽  
Shigeru Miyagawa ◽  
Haruhiko Kondoh ◽  
Naomasa Kawaguchi ◽  
...  

2017 ◽  
Vol 2 (3) ◽  
pp. 285-296 ◽  
Author(s):  
Joseph C. McCarthy ◽  
Mark Aronovitz ◽  
Jennifer J. DuPont ◽  
Timothy D. Calamaras ◽  
Iris Z. Jaffe ◽  
...  

2002 ◽  
Vol 283 (1) ◽  
pp. H339-H345 ◽  
Author(s):  
Takayuki Saito ◽  
Fu Hu ◽  
Lara Tayara ◽  
Linda Fahas ◽  
Hani Shennib ◽  
...  

Strong expression of the inducible form of nitric oxide synthase (NOS II) has been shown in the myocardium of patients with myocardial infarction (MI). We hypothesized that NOS II plays an important role in the development of MI and subsequent heart failure and that inhibition of NOS II may beneficially alter the course of the disease. Long-term administration (2 mo) of the selective NOS II inhibitor S-methylisothiourea (SMT) to rats with MI significantly improved cardiac function. A significant drop in mortality, lung water content, infarct size, and cardiomyocyte hypertrophy was also associated with the use of SMT. Plasma concentration of nitrite and nitrate was also reduced by SMT. Short-term administration of SMT (first 2 wk only) significantly reduced infarct size; however, it did not improve cardiac dysfunction measured 2 mo after MI. These findings demonstrate that induction of NOS II during MI exerts negative effects on cardiac function and structure. Long-term administration of a selective NOS II inhibitor may prove to be beneficial in the treatment of MI and congestive heart failure.


Sign in / Sign up

Export Citation Format

Share Document