Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 104, Issue 39, Pages 15560-15565Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0705891104
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Funding
- NHLBI NIH HHS [R01 HL060849, 2R01 HL060849-07] Funding Source: Medline
- NIDDK NIH HHS [1F32 DK077380-01, F32 DK077380, R01 DK064344] Funding Source: Medline
- NIGMS NIH HHS [R21 GM073049, R21 GM73049-01] Funding Source: Medline
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The recent discovery that hydrogen sulfide (H2S) is an endogenously produced gaseous second messenger capable of modulating many physiological processes, much like nitric oxide, prompted us to investigate the potential of H2S as a cardioprotective agent. In the current study, we demonstrate that the delivery of H2S 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 H2S by cardiac-specific overexpression of cystathionine gamma-lyase (alpha-MHC-CGL-Tg mouse) significantly limits the extent of injury. These findings demonstrate that H2S may be of value in cytoprotection during the evolution of myocardial infarction and that either administration of H2S or the modulation of endogenous production may be of clinical benefit in ischemic disorders.
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