Ammonia neutralization in heart muscle

Писаренко, О. И.; Minkovskii, E. B.; Студнева, И. М.

doi:10.1007/bf00834227

Cited by 2 publications

(2 citation statements)

References 5 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…While increased cardiac ammonia production generally does not appear to be found in the coronary sinus of patients with heart failure, it is clear that the myocardium produces ammonia during stress, injury, death and necrosis (11). Even though average coronary arteriovenous differences in ammonia are not found in patients with heart failure, concentrations of ammonia are likely highest in the interstitial space near the site of injury or stress (30,37), and local ammonia neutralization capacity may be exceeded.…”

Section: Ammonia and The Heartmentioning

confidence: 99%

“…Rat hearts perfused with nitrogen 15 isotope over a range of ammonia concentrations demonstrate ammonia neutralization primarily by glutamic acid with glutamine formation. Isoproterenol-induced necrosis led to an elevated tissue ammonia with a decrease in ammonia neutralization (30). Myocardial protection was improved by glutamic acid addition to the isolated perfused rat heart during 30-min ischemic arrest and resulted in less ammonia accumulation and improved functional recovery, although ammonia levels remained high (29).…”

Section: Ammonia and The Heartmentioning

confidence: 99%

See 1 more Smart Citation

Hypothesis: role for ammonia neutralization in the prevention and reversal of heart failure

Bing

2018

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Ammonia plays a central role in the life and death of all living organisms and has been studied for over 100 yr. Ammonia is necessary for growth and development, but it is toxic in excess, and, as a result, differing methods of ammonia neutralization have evolved. After physiological and pathological stress to the heart, tissue ammonia levels rise. Local ammonia neutralization may be inadequate, and excess ammonia may exert its toxic effects. Phenylbutyrate (PBA), which is Federal Drug Administration approved for the treatment of elevated blood ammonia in urea cycle disorders, provides an accessory pathway for ammonia excretion. Recently, PBA has also been found to prevent specific cardiomyopathies. The central theme presents the hypothesis that stress to the myocardium from a variety of environmental sources causes injury, cell death, necrosis, and ammonia production. Ammonia, if not neutralized, exerts downstream toxic effects. Here, data are presented showing that neutralization with PBA alone and PBA combined with angiotensin-converting enzyme inhibition prevent and reverse pathophysiology associated with specific cardiomyopathies. NEW & NOTEWORTHY Ammonia produced after myocardial injury is hypothesized to be an upstream stress contributing to the pathophysiology of heart failure, effects that may be attenuated by a documented ammonia-reducing treatment. Reversal of heart failure can be achieved using an angiotensin-converting enzyme inhibitor combined with an ammonia-reducing treatment.

show abstract

Section: Ammonia and The Heartmentioning

confidence: 99%

Section: Ammonia and The Heartmentioning

confidence: 99%