Intravenous administration of CoQ10 evokes increase in NO-mediated blood vessels relaxationстатья Исследовательская статья

Статья опубликована в высокорейтинговом журнале

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Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 28 октября 2016 г.

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[1] Intravenous administration of coq10 evokes increase in no-mediated blood vessels relaxation / O. Medvedev, L. Kozaeva, E. Gorodetskaya, E. Kalenikova // European Journal of Heart Failure. — 2016. — Vol. 18. — P. 426–426. Introduction: The presence of endothelial dysfunction is associated with an increased mortality risk in patientswith chronic heart failure. Coenzyme Q10 (CoQ10) is recommended for treatment of patients with congestive heart failure, but due to its low bioavailability it is necessary long term administration in order to reach therapeutical effect. One of the proposed mechanisms of beneficial effects of Coq10 is improvement in the vasodilating NO-mediated function of endothelium. Purpose: Investigation of the fast effects of CoQ10, administered intravenously, on the NO-mediated vasorelaxation, evoked by acetylcholine. Methods. Male Wistar rats (300-350g) were anaesthetized with chloralhydrate (400 mg/kg, ip) and placed on a heated surgical pad at constant body temperature 37±0.5 ∘C. 3% water-based solution of CoQ10 (30 mg/kg) or saline (0.9% NaCl, 1 mL/kg) were administered intravenously via the femoral vein. 2 h after drugs administration the animals were anaesthetized by chloralhydrate over dose (600 mg kg−1, ip) and decapitated. The descending thoracic aorta was carefully excised and cut into ring segments 3 mm in length and then transferred into 10-ml organ baths containing Krebs solution bubbled with a mixture of 95% O2 and 5% CO2. The rings were precontracted with 0.3 micromolar Phenylephine (PE), and after a steady-state tension had been reached, increasing concentrations of ACh (0.001 micromolar - 30 micromolar) were cumulatively added to the organ bath. Results: ACh elicited a concentration-dependent relaxation of rat aortic rings. The maximum relaxation (E max, %) was obtained at a Ach concentration of 30 micromolar. In the CoQ10-treated group the relaxant responses to ACh were markedly potentiated when compared with the control (saline) group (94.2±2.0% vs 68.1±4.4%, respectively, p<0.01). It was significant difference in pD2 (-lg EC50, ) values of the control and treatment groups (5.79±0.29 vs 8.14±0.65, p<0.05). Conclusion: 2h duration of CoQ10 (30 mg/kg) action is enough for improving the vasodilating NO-mediated function of endothelium. This mechanism could be partially responsible for positive effects of CoQ10 in congestive heart failure.

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