Open AccessHydrogen sulfide-mediated cardioprotection against ischemia reperfusion is linked to KATP channel for mitochondrial preservation but not for its distinct preference on interfibrillar mitochondria
Author(s) -
Priyadharshini Chandrasekaran,
Sriram Ravindran,
Sri Rahavi Boovarahan,
Gino A. Kurian
Publication year - 2019
Publication title -
bangladesh journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.385
H-Index - 23
eISSN - 1991-0088
pISSN - 1991-007X
DOI - 10.3329/bjp.v14i2.39890
Subject(s) - cardioprotection , mitochondrion , glibenclamide , diazoxide , ischemia , reperfusion injury , hydrogen sulfide , pharmacology , chemistry , medicine , microbiology and biotechnology , endocrinology , biochemistry , biology , diabetes mellitus , insulin , sulfur , organic chemistry
Hydrogen sulfide has been shown to protect myocardium against ischemia-reperfusion injury by preserving interfibrillar mitochondria functional activi-ties than subsarcolemmal mitochondria. In this study, the role of the KATP channel in modulating the mitochondrial subpopulations during the cardioprotection mediated by NaSH (H2S donor) was investigated. Isolated rat hearts were treated with mitochondrial KATP channel closer glibenclamide (10 μM)/opener diazoxide (0.8 mM) via Langendorff perfusion apparatus before ischemia-reperfusion. The results showed that NaSH pre-conditioning in presence of glibenclamide significantly improved cardiac recovery without any significant difference between interfibrillar mitochondria and subsarcolemmal mitochondria. In conclusion, targeting KATP channel may not be good option to target interfibrillar mitochondria/subsarcolemmal mitochondria against ischemia-reperfusion injury.