Cookies help us deliver our services. By using our services, you agree to our use of cookies. More information

Kancirova 2016 Physiol Res

From Bioblast
Publications in the MiPMap
Kancirová I, Jašová M, Muráriková M, Sumbalová Z, Uličná O, Ravingerová T, Waczulíková I, Ziegelhöffer A, Ferko M (2016) Cardioprotection induced by remote ischemic preconditioning preserves the mitochondrial respiratory function in acute diabetic myocardium. Physiol Res 65:S611-19.

» PMID: 28006943 Open Access

Kancirova I, Jasova M, Murarikova M, Sumbalova Z, Ulicna O, Ravingerova T, Waczulikova I, Ziegelhoeffer A, Ferko M (2016) Physiol Res

Abstract: A 2×2 factorial design was used to evaluate possible preservation of mitochondrial functions in two cardioprotective experimental models, remote ischemic preconditioning and streptozotocin-induced diabetes mellitus, and their interaction during ischemia/reperfusion injury (I/R) of the heart. Male Wistar rats were randomly allocated into four groups: control (C), streptozotocin-induced diabetic (DM), preconditioned (RPC) and preconditioned streptozotocin-induced diabetic (DM+RPC). RPC was conducted by 3 cycles of 5-min hind-limb ischemia and 5-min reperfusion. DM was induced by a single dose of 65 mg/kg streptozotocin. Isolated hearts were exposed to ischemia/reperfusion test according to Langendorff. Thereafter mitochondria were isolated and the mitochondrial respiration was measured. Additionally, the ATP synthase activity measurements on the same preparations were done. Animals of all groups subjected to I/R exhibited a decreased state 3 respiration with the least change noted in DM+RPC group associated with no significant changes in state 2 respiration. In RPC, DM and DM+RPC group, no significant changes in the activity of ATP synthase were observed after I/R injury. These results suggest that the endogenous protective mechanisms of RPC and DM do preserve the mitochondrial function in heart when they act in combination. Keywords: Myocardial preconditioning, Mitochondria, Energy metabolism, Mitochondrial ATP synthase, Myocardial ischemic reperfusion injury Bioblast editor: Sumbalova Z, Kandolf G O2k-Network Lab: SK Bratislava Sumbalova Z


Labels: MiParea: Respiration  Pathology: Diabetes  Stress:Ischemia-reperfusion  Organism: Rat  Tissue;cell: Heart  Preparation: Isolated mitochondria  Enzyme: Complex V;ATP synthase 

Coupling state: LEAK, OXPHOS  Pathway: F, N  HRR: Oxygraph-2k