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Acta Physiologica Congress

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Acta Physiologica 2007; Volume 191, Supplement 658
Joint Meeting of The Slovak Physiological Society, The Physiological Society and The Federation of European Physiological Societies
9/11/2007-9/14/2007
Bratislava, Slovakia


SUSCEPTIBILITY TO ISCHAEMIA-INDUCED ARRHYTHMIAS AND THE EFFECT OF MITOCHONDRIAL KATP CHANNELS ACTIVATION AND ANTIOXIDANT TREATMENT IN THE DIABETIC RAT HEART
Abstract number: PW03-16

Matejikova1 J., Ondrejcakova1 M., Pancza1 D., Blazickova1 I., Formankova1 I., Ravingerova1 T.

1Institute of Heart Research, Slovak Acad. Sci., Bratislava, Slovakia

Aims: 

Opening of mitochondrial KATP channels (mKATP) interacting with free radicals is suggested as a key element in antiischaemic protection in the normal heart, while its role in diabetes mellitus (DM) is unclear. The aims were to characterise ischaemia-induced arrhythmias and effects of N-acetylcysteine (NAC) and mKATP opener diazoxide (D) in the diabetic rat heart.

Methods: 

Seven days after streptozotocin injection, Langendorff-perfused hearts were subjected to 30min occlusion of the LAD coronary artery with or without 15min treatment with D (50mM) or NAC (4mM).

Results: 

Total number of ventricular premature beats (VPB) was lower in the DM group. Similarly, number of episodes and duration of ventricular tachycardia (VT) were reduced to 6.1 ± 3.7 and 1.8 ± 0.6s (from 12.1 ± 2.4 and 3.4 ± 0.5s, resp., in non-DM controls; P < 0.05). Both, D and NAC were antiarrhythmic in non-DM group. In the diabetics, D further suppressed arrhythmias (VT 0.6 ± 0.4 and 0.4 ± 0.2s; P < 0.05 vs. non-treated DM), while NAC did not modify arrrhythmogenesis (VT 6.2 ± 2.6 and 2.8 ± 1.2s; P > 0.05 vs. non-treated DM).

Conclusions: 

Early period of DM is associated with enhanced resistance to ischaemia-induced arrhythmias facilitated by mKATP opening. DM might induce adaptive processes in the myocardium that reduce susceptibility to antioxidant treatment. Grants VEGA SR 2/5110/25, APVT 51-027404.

GroupsVPB (total number)  
 C D NAC
Non-diabetic 538 ± 58 168 ± 22*290 ± 52*
Diabetic 224 ± 53*71 ± 24*†207 ± 51*
*– P < 0.05 vs. non-diabetics controls; †– P < 0.05 vs. non-treated diabetics

To cite this abstract, please use the following information:
Acta Physiologica 2007; Volume 191, Supplement 658 :PW03-16

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