Hydrogen sulfide induce negative inotropic effect in isolated hearts via KATP channel and mitochondria membrane KATP channel
Sun, Y.; Zhang, S.-Q.; Jin, H.-F.; Tang, C.-S.; Du, J.-B.
Zhonghua Xin Xue Guan Bing Za Zhi 37(2): 161-164
2009
ISSN/ISBN: 0253-3758 PMID: 19719997 Document Number: 630201
Hydrogen sulfide (H(2)S) dilates blood vessels in vivo and in vitro probably by opening vascular smooth muscle K(+)-ATP channels. The study was designed to observe the role of mitochondria membrane K(ATP) channel blocker (5-HD) in the regulation of cardiac function isolated perfused heart of rat with H(2)S. The isolated rat heart was perfused in a Langendorff apparatus. After 20 minutes of stabilization, physiological concentration of NaHS (H(2)S donor, 100 micromol/L) was continuously perfused for 20 min in group A (n = 6), isolated hearts in group B (n = 6) and C (n = 7) were pretreated with nonspecific K(ATP) channel blocker glibenclamide (100 micromol/L) or 5-HD (100 micromol/L) for 5 minutes then perfused with NaHS (100 micromol/L) for 10 minutes. Heart rate (HR), left ventricular developed pressure (DeltaLVP), dp/dt(max) and dp/dt(min) and coronary perfusion flow (CPF) were measured. Post continuous perfusion of NaHS at physiological concentration for 20 minutes, DeltaLVP, dp/dt(max) and dp/dt(min) all significantly decreased while HR and CPF remained unchanged compared to baseline levels (all P < 0.05). The negative inotropic effect of H(2)S could partly be blocked by nonspecific K(ATP) channel blocker glibenclamide and mitochondria membrane K(ATP) channel blocker 5-HD. Present findings suggested that H(2)S at physiological concentration could produce negative inotropic effect in isolated hearts and this effect was mediated by K(ATP) channel and mitochondria membrane K(ATP) channel.