Protection against ischemia-induced ventricular arrhythmias and myocardial dysfunction conferred by preconditioning in the rat heart: involvement of mitochondrial K(ATP) channels and reactive oxygen species
Jazyk angličtina Země Česko Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
18198991
DOI
10.33549/physiolres.931317
PII: 1317
Knihovny.cz E-zdroje
- MeSH
- acetylcystein farmakologie MeSH
- antiarytmika farmakologie MeSH
- antioxidancia farmakologie MeSH
- blokátory draslíkových kanálů farmakologie MeSH
- časové faktory MeSH
- diazoxid farmakologie MeSH
- draslíkové kanály účinky léků metabolismus MeSH
- funkce levé komory srdeční * účinky léků MeSH
- hydroxykyseliny farmakologie MeSH
- ischemické přivykání * MeSH
- komorové extrasystoly metabolismus patofyziologie prevence a kontrola MeSH
- kontrakce myokardu * účinky léků MeSH
- krysa rodu Rattus MeSH
- kyseliny dekanové farmakologie MeSH
- látky reagující s kyselinou thiobarbiturovou metabolismus MeSH
- myokard metabolismus MeSH
- obnova funkce MeSH
- oxidační stres MeSH
- perfuze MeSH
- peroxidace lipidů MeSH
- potkani Wistar MeSH
- reaktivní formy kyslíku metabolismus MeSH
- reperfuzní poškození myokardu metabolismus patofyziologie prevence a kontrola MeSH
- techniky in vitro MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- 5-hydroxydecanoic acid MeSH Prohlížeč
- acetylcystein MeSH
- antiarytmika MeSH
- antioxidancia MeSH
- blokátory draslíkových kanálů MeSH
- diazoxid MeSH
- draslíkové kanály MeSH
- hydroxykyseliny MeSH
- kyseliny dekanové MeSH
- látky reagující s kyselinou thiobarbiturovou MeSH
- mitochondrial K(ATP) channel MeSH Prohlížeč
- reaktivní formy kyslíku MeSH
Ischemic preconditioning (I-PC) induced by brief episodes of ischemia and reperfusion (I/R) protects the heart against sustained I/R. Although activation of mitochondrial K(ATP) channels (mitoK(ATP)) interacting with reactive oxygen species (ROS) has been proposed as a key event in this process, their role in the antiarrhythmic effect is not clear. This study was designed: 1) to investigate the involvement of mito K(ATP) opening in the effect of I-PC (1 cycle of I/R, 5 min each) on ventricular arrhythmias during test ischemia (TI, 30-min LAD coronary artery occlusion) in Langendorff-perfused rat hearts and subsequent postischemic contractile dysfunction, and 2) to characterize potential mechanisms of protection conferred by I-PC and pharmacological PC induced by mito K(ATP) opener diazoxide (DZX), with particular regards to the modulation of ROS generation. Lipid peroxidation (an indicator of increased ROS production) was determined by measurement of myocardial concentration of conjugated dienes (CD) and thiobarbituric acid reactive substances (TBARS) in non-ischemic controls, non-preconditioned and preconditioned hearts exposed to TI, I-PC alone, as well as after pretreatment with DZX, mito K(ATP) blocker 5-hydroxydecanoate (5-HD) and antioxidant N-acetylcysteine (NAC). Total number of ventricular premature beats (VPB) that occurred in the control hearts (518+/-71) was significantly (P<0.05) reduced by I-PC (195+/-40), NAC (290+/-56) and DZX (168+/-22). I-PC and NAC suppressed an increase in CD and TBARS caused by ischemia indicating lower production of ROS. On the other hand, I-PC and DZX themselves moderately enhanced ROS generation, prior to TI. Bracketing of I-PC with 5-HD suppressed both, ROS production during PC and its cardioprotective effect. In conclusion, potential mechanisms of protection conferred by mito K(ATP) opening in the rat heart might involve a temporal increase in ROS production in the preconditioning phase triggering changes in the pro/antioxidant balance in the myocardium and attenuating ROS production during subsequent prolonged ischemia.
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