The Annals of thoracic surgery · 2013
Vasorelaxation induced by new third-generation dihydropyridine calcium antagonist azelnidipine in human internal mammary artery.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Gao Ge, Liu Xiao-Cheng, Jing Wen-Bin, Yang Qin, He Guo-Wei
Аннотация
BACKGROUND: Graft spasm remains challenging in coronary artery bypass graft (CABG) surgery. Calcium antagonists are commonly used in patients with coronary artery disease. We investigated the inhibitory effect of the new third-generation dihydropyridine calcium antagonist azelnidipine on the vasoconstriction in human internal mammary artery (IMA) from patients undergoing CABG.
METHODS: Isolated IMA rings (n = 68, taken from 28 patients) were studied in myograph in two ways: the relaxing effect of azelnidipine on vasoconstrictor-induced precontraction by potassium chloride (KCl) and U46619; and the depressing effect of azelnidipine at plasma concentrations on the contraction.
RESULTS: Azelnidipine caused full relaxation in KCl-contracted (96.5% ± 0.7%) and in U46619-contracted (96.5% ± 1.4%) IMA rings (n = 8), with 28.8-fold higher potency to KCl than to U46619 (EC50 -7.49 ± 0.21 versus -6.03 ± 0.11 log M, p < 0.01). Pretreatment of IMA with plasma concentrations of azelnidipine (-6.1 log M) significantly depressed subsequent contraction to KCl (from 25.8 ± 2.2 mN to 16.0 ± 1.5 mN, p < 0.01) and U46619 (from 30.6 ± 4.0 mN to 16.5 ± 2.2 mN, p < 0.05).
CONCLUSIONS: We conclude that in human IMA, azelnidipine has a potent inhibitory effect on the vasoconstriction mediated by a variety of vasoconstrictors. Thus, use of azelnidipine in CABG patients is favored for treating and preventing graft spasm.
METHODS: Isolated IMA rings (n = 68, taken from 28 patients) were studied in myograph in two ways: the relaxing effect of azelnidipine on vasoconstrictor-induced precontraction by potassium chloride (KCl) and U46619; and the depressing effect of azelnidipine at plasma concentrations on the contraction.
RESULTS: Azelnidipine caused full relaxation in KCl-contracted (96.5% ± 0.7%) and in U46619-contracted (96.5% ± 1.4%) IMA rings (n = 8), with 28.8-fold higher potency to KCl than to U46619 (EC50 -7.49 ± 0.21 versus -6.03 ± 0.11 log M, p < 0.01). Pretreatment of IMA with plasma concentrations of azelnidipine (-6.1 log M) significantly depressed subsequent contraction to KCl (from 25.8 ± 2.2 mN to 16.0 ± 1.5 mN, p < 0.01) and U46619 (from 30.6 ± 4.0 mN to 16.5 ± 2.2 mN, p < 0.05).
CONCLUSIONS: We conclude that in human IMA, azelnidipine has a potent inhibitory effect on the vasoconstriction mediated by a variety of vasoconstrictors. Thus, use of azelnidipine in CABG patients is favored for treating and preventing graft spasm.