Chronic Administration of Coenzyme Q₁₀ Limits Postinfarct Myocardial Remodeling in Rats

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E. I. Kalenikova^*, E. A. Gorodetskaya, E. G. Kolokolchikova, D. A. Shashurin, and O. S. Medvedev

Faculty of Basic Medicine, Lomonosov Moscow State University, Lomonosovsky pr. 31/5, 117192 Moscow, Russia; fax: (495) 939-2423; E-mail: eikaleni@fbm.msu.ru

^* To whom correspondence should be addressed.

Received September 28, 2006

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The effect of chronic coronary artery occlusion on the content of rat myocardial coenzymes Q (CoQ) and evaluation of the applicability of CoQ₁₀ for limiting postinfarct remodeling have been investigated. Left ventricle myocardium hypertrophy was characterized by the decrease in CoQ₉ (-45%, p < 0.0001), CoQ₁₀ (-43%, p < 0.001), and alpha-tocopherol (-35%, p < 0.05). There were no differences between the parameters of postinfarction and sham-operated rats in plasma. Administration of CoQ₁₀ (10 mg/kg) via a gastric probe for 3 weeks before and 3 weeks after occlusion maintained higher levels of CoQ in the postinfarction myocardium: the decrease in CoQ₉ and CoQ₁₀ was 25% (p < 0.05) and 23% (p < 0.05), respectively (versus sham-operated animals). Plasma concentrations of CoQ₁₀ were more than 2 times higher (p < 0.05). In CoQ treated rats there was significant correlation between plasma levels of CoQ and the infarct size: r = -0.723 (p < 0.05) and r = -0.839 (p < 0.01) for CoQ₉ and CoQ₁₀. These animals were also characterized by earlier and more intensive scar tissue formation in the postinfarction myocardium and also by more pronounced cell regeneration processes. This resulted in the decrease in both the infarct size (16.2 ± 8.1 vs. 27.8 ± 12.1%) and also mass index of left ventricle (2.18 ± 0.24 vs. 2.38 ± 0.27 g/kg) versus untreated rats (p < 0.05). Thus, long-term treatment with ubiquinone increases plasma and myocardial CoQ content and this can improve the survival of myocardial cells during ischemia and limit postinfarct myocardial remodeling.

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KEY WORDS: coenzyme Q, ischemia, infarct, myocardium, hypertrophy, HPLC, cardioprotection

DOI: 10.1134/S0006297907030121

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