Zobrazeno 1 - 7
of 7
pro vyhledávání: '"Nidas A. Undrovinas"'
Autor:
Mikhail S. Novikov, A A Abramov, Alexander A. Makarov, Vladimir A. Mitkevich, Irina Yu. Petrushanko, Valentina A. Lakunina, Yuri M. Poluektov, Asker Y. Khapchaev, Vladimir P. Shirinsky, Valery I. Kapelko, Vladimir L. Lakomkin, Nidas A. Undrovinas
Publikováno v:
Scientific Reports
Scientific Reports, Vol 9, Iss 1, Pp 1-12 (2019)
Scientific Reports, Vol 9, Iss 1, Pp 1-12 (2019)
Severe hypoxia leads to decline in cardiac contractility and induces arrhythmic events in part due to oxidative damage to cardiomyocyte proteins including ion transporters. This results in compromised handling of Ca2+ ions that trigger heart contract
Autor:
Sudhish Mishra, Victor A. Maltsev, Hani N. Sabbah, Nidas A. Undrovinas, Albertas I. Undrovinas, Vitaliy Reznikov
Publikováno v:
The Journal of Physiology. 593:1409-1427
Late Na+ current (INaL) contributes to action potential (AP) duration and Ca2+ handling in cardiac cells. Augmented INaL was implicated in delayed repolarization and impaired Ca2+ handling in heart failure (HF). We tested if Na+ channel (Nav) neurona
Autor:
Vladimir L. Lakomkin, Elena V Lukoshkova, Valery I. Kapelko, Nidas A. Undrovinas, Vladimir P. Shirinsky, Asker Y. Khapchaev, A A Abramov
Publikováno v:
Oxidative Medicine and Cellular Longevity, Vol 2017 (2017)
Oxidative Medicine and Cellular Longevity
Oxidative Medicine and Cellular Longevity
Background. Nitric oxide can successfully compete with oxygen for sites of electron-transport chain in conditions of myocardial hypoxia. These features may prevent excessive oxidative stress occurring in cardiomyocytes during sudden hypoxia-reoxygena
Autor:
Sudhish Mishra, Albertas I. Undrovinas, Victor A. Maltsev, Vitaliy Reznikov, Hani N. Sabbah, Nidas A. Undrovinas
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 301:H1596-H1605
The emerging paradigm for Na+ current in heart failure (HF) is that its transient component ( INaT) responsible for the action potential (AP) upstroke is decreased, whereas the late component ( INaL) involved in AP plateau is augmented. Here we teste
Autor:
Hani N. Sabbah, Vitaliy Reznikov, Victor A. Maltsev, Albertas I. Undrovinas, Nidas A. Undrovinas
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 294:H1597-H1608
Augmented and slowed late Na+ current ( INaL) is implicated in action potential duration variability, early afterdepolarizations, and abnormal Ca2+ handling in human and canine failing myocardium. Our objective was to study INaL modulation by cytosol
Autor:
Luiz Belardinelli, Albertas I. Undrovinas, Victor A. Maltsev, Hani N. Sabbah, Nidas A. Undrovinas
Publikováno v:
The journal of physiological sciences : JPS. 60(4)
We elucidate the role of late Na+ current (INaL) for diastolic intracellular Ca2+ (DCa) accumulation in chronic heart failure (HF). HF was induced in 19 dogs by multiple coronary artery microembolizations; 6 normal dogs served as control. Ca2+ transi
Publikováno v:
Journal of the American College of Cardiology. (5):A178