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Am J Physiol Heart Circ Physiol (February 14, 2002). doi:10.1152/ajpheart.00596.2001
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Articles in PresS, published online ahead of print February 14, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00596.2001
Submitted on July 10, 2001
Accepted on February 1, 2002

Inhibition of NO synthase II prevents cardiac dysfunction in myocardial infarction and congestive heart failure

Takayuki Saito1, Fu Hu1, Lara Tayara1, Linda Fahas1, Hani Shennib1, and Adel Giaid1*

1 Pathology, Medicine, and Cardiothoracic Surgery, Montreal General Hospital and McGill University, Montreal, Quebec, Canada

* To whom correspondence should be addressed. E-mail: saitotjk{at}hotmail.com.

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 (2 months) administration of a selective NOS II inhibitor, S-methylisothiourea (SMT) to the 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 weeks only) significantly reduced infarct size; however, it did not improve cardiac dysfunction measured at 2 months 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.




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