Objectives: Upregulation of arginase redirects the arginine metabolism from nitric oxide (NO) synthesis to the formation of polyamine and proline, thus causing cardiac dysfunction. NO synthesis is also impaired by asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase inhibitor. We aimed to evaluate the impact of arginase and ADMA levels on left ventricular function after myocardial infarction (MI).
Design and methods: Blood samples from 43 MI patients and 33 controls were used. Arginase I and TNF-α were quantified by ELISA; arginine, ADMA and homocysteine concentrations by HPLC; and high-sensitive CRP by immunoassay techniques.
Results: Arginase concentrations were higher in MI patients than in controls (121 ± 73 ng/mL vs 58 ± 41, p = 0.001) and were negatively associated with left ventricular ejection fraction (r = -0.467, p = 0.019). Significantly low arginine/ADMA ratio was observed in MI patients.
Conclusion: Induced arginase I after myocardial infarction may deplete the arginine pool. The changes related to arginine metabolism may have a role in ventricular dysfunction.
Copyright © 2011. Published by Elsevier Inc.