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• W2279432365 abstract "We determined whether flumazenil mimics ischemic preconditioning in chick cardiomyocytes and examined the role of intracellular reactive oxygen species (ROS) and ATP-dependent potassium (K ATP ) channels in mediating the effect. Chick ventricular myocytes were perfused with a balanced salt solution in a flow-through chamber. Cell viability was quantified using propidium iodide, and ROS generation was assessed using the reduced form of 2′,7′-dichlorofluorescin (DCFH). Cells were exposed to 1 h of simulated ischemia and 3 h of reoxygenation. Preconditioning was initiated with 10 min of ischemia followed by 10 min of reoxygenation. Alternatively, flumazenil was added to the perfusate for 10 min and removed 10 min before the start of ischemia. Flumazenil (1 and 10 μM) and preconditioning reduced cell death [54 ± 5%, n = 3; 26 ± 4%, n = 6 ( P < 0.05); and 20 ± 2%, n = 6 (P < 0.05), respectively, vs. 57 ± 7%, n = 10, in controls] and increased DCFH oxidation (an index of ROS production) [0.35 ± 0.11, n = 3; 2.64 ± 0.69, n = 8 ( P < 0.05); and 2.46 ± 0.52, n = 6 ( P< 0.05), respectively, vs. 0.26 ± 0.05, n = 9, in controls]. Protection and increased ROS signals with flumazenil (10 μM) were abolished with the thiol reductant N-(2-mercaptopropionyl)-glycine (2-MPG, 800 μM), an antioxidant (cell death: 2-MPG + flumazenil, 55 ± 12%, n = 6; ROS signals: 2-MPG + flumazenil, 0.11 ± 0.19, n = 6). Treatment with 5-hydroxydecanoate (1 mM), a selective mitochondrial K ATP channel antagonist, abolished its protection. These results demonstrate that flumazenil mimics preconditioning to reduce cell death in myocytes. ROS signals with the resultant mitochondrial K ATP channel activation are important components of the intracellular signaling pathway of flumazenil." @default.
• W2279432365 created "2016-06-24" @default.
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• W2279432365 date "2000-10-01" @default.
• W2279432365 modified "2023-09-27" @default.
• W2279432365 title "Flumazenil preconditions cardiomyocytes via oxygen radicals and K_ATPchannels" @default.
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• W2279432365 doi "https://doi.org/10.1152/ajpheart.2000.279.4.h1858" @default.
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