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Acta Physiologica 2012; Volume 206, Supplement 691
Scandinavian Physiological Society's Annual Meeting
8/24/2012-8/26/2012
Helsinki, Finland
EFFECTS OF ECHINOCHROME ON VENTRICULAR REPOLARIZATION IN EXPERIMENTAL ISCHEMIA AND REPERFUSION
Abstract number: P51
SEDOVA1 KA, BERNIKOVA1 OG, KHARIN1 SN
1Laboratory of Cardiac Physiology, Institute of Physiology, Komi Science Centre, Ural Branch, Russian Academy of Sciences, Syktyvkar, Russia; Komi Branch of the Kirov State Medical Academy, Syktyvkar, Russia
The effects of echinochrome (Ech), an antioxidant, on ventricular repolarization were studied in a cat model of 30 min ischemia / 30 min reperfusion. Forty-eight left ventricular unipolar electrograms were simultaneously recorded using plunge needle electrodes at baseline, 30 min after ligation of the left anterior descending coronary artery, and 30 min of reperfusion. Synthetic Ech (1 mg/kg i.v.) provided by the Pacific Institute of Bioorganic Chemistry of the Far Eastern Branch of the RAS (Vladivostok, Russia) was infused 5 min before occlusion or reperfusion. Activation-recovery intervals (ARIs) were measured for each lead and corrected to heart rate. Ech administered prior to coronary occlusion decreased ischemia-induced shortening of ARIs in the ischemic area (from 231±40 to 182±21 ms vs. from 221±33 to 163±32 ms in the controls, p<0.05; p<0.05 vs. respective baseline) and tended to decrease ischemia-induced increasing of the global ARI dispersion (from 74±15 to 111±20 ms vs. from 73±10 to 133±33 ms in the controls, NS; p<0.05 vs. respective baseline). Ech given prior to reperfusion inhibited the restoration of ARIs in the ischemic area (175±61 ms vs. 238±46 ms in the controls, p<0.05; p<0.05 vs. respective baseline and occlusion) and the restoration of the global ARI dispersion (137±26 ms vs. 86±28 ms in the controls, p<0.05; Ech: p<0.05 vs. baseline; control: p<0.05 vs. occlusion) during reperfusion. Ech did not affect ARIs in the non-ischemic area. This study demonstrates that Ech is a cardioprotective agent in the acute phase of ischemia by diminishing alterations of ventricular repolarization in the ischemic area. This work was supported by the Ural Branch of the RAS (project No. 12-C-4-1009).
To cite this abstract, please use the following information:
Acta Physiologica 2012; Volume 206, Supplement 691 :P51