Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function
Albert Einstein College of Medicine · National Center of Neurology and Psychiatry · +5 more institutions
Abstract
The recent discovery that hydrogen sulfide (H(2)S) is an endogenously produced gaseous second messenger capable of modulating many physiological processes, much like nitric oxide, prompted us to investigate the potential of H(2)S as a cardioprotective agent. In the current study, we demonstrate that the delivery of H(2)S at the time of reperfusion limits infarct size and preserves left ventricular (LV) function in an in vivo model of myocardial ischemia-reperfusion (MI-R). This observed cytoprotection is associated with an inhibition of myocardial inflammation and a preservation of both mitochondrial structure and function after I-R injury. Additionally, we show that modulation of endogenously produced H(2)S…
Citation impact
- FWCI
- 70.29
- Percentile
- 100%
- References
- 42
Authors
13- JWJohn W. Elrod
Albert Einstein College of Medicine, National Center of Neurology and Psychiatry
- JWJohn W. Calvert
National Center of Neurology and Psychiatry
- JMJo Morrison
University Hospital, Newark, University of Alabama at Birmingham
- JEJeannette E. Doeller
University Hospital, Newark, University of Alabama at Birmingham
- DWDavid W. Kraus
University Hospital, Newark, University of Alabama at Birmingham
Topics & keywords
- Cytoprotection
- Reperfusion injury
- Nitric oxide
- Ischemia
- Myocardial infarction
- In vivo
- Pharmacology
- Chemistry
- Good health and well-being