ВЛИЯНИЕ ДОКСОРУБИЦИНА НА РЕАКТИВНОСТЬ БРЫЖЕЕЧНЫХ АРТЕРИЙ КРЫС ВИСТАР
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Ключевые слова

доксорубицин
брыжеечная артерия
эндотелий
ацетилхолин-индуцированная дилатация
вазоконстрикция
фенилэфрин
нитропруссид

Как цитировать

Иванова, Г. Т. (2022). ВЛИЯНИЕ ДОКСОРУБИЦИНА НА РЕАКТИВНОСТЬ БРЫЖЕЕЧНЫХ АРТЕРИЙ КРЫС ВИСТАР. Российский физиологический журнал им. И. М. Сеченова, 108(11), 1453–1467. https://doi.org/10.31857/S0869813922110036

Аннотация

Доксорубицин применяется в качестве противоопухолевого препарата, однако он оказывает негативное влияние на сердечно-сосудистую систему.  Основное внимание уделяется кардиотоксическому эффекту, а механизмы его действия на сосуды изучены недостаточно. В исследовании оценивалось влияние доксорубицина на реактивность брыжеечных артерий крыс.

Экспериментальной группе крыс Вистар вводили однократно внутрибрюшинно доксорубицин (4мг/кг), контрольным животным - физиологический раствор в равном объеме. Через 6 недель исследовали реактивность брыжеечных артерий на ацетилхолин (АХ), нитропруссид и фенилэфрин. Для уточнения механизмов эндотелийзависимой вазодилатации использовали блокаторы: NO-синтазы - L-NAME, циклооксигеназы – индометацин, К+-каналов – тетраэтиламмоний. Для оценки реактивности артерий in vivo проводили микрофото- и видеорегистрацию диаметра брыжеечных артерий крыс  (микроскоп Биомед МС-1Т-ZOOM и камера Basler BASLER acA4600-10uc), полученные данные обрабатывали в программе MultiMedia Catаlog. Показано, что доксорубицин модифицировал реактивность брыжеечных артерий крыс: повышал констрикторные реакции фенилэфрина и угнетал эндотелийзависимую вазорелаксацию при действии АХ. При этом введение крысам доксорубицина приводило к снижению эффективности NO-зависимых механизмов регуляции тонуса сосудов (оцененных по разнице в амплитуде АХ-индуцированной вазодилатации до и после применения L-NAME), а также к уменьшению вызванной нитропруссидом релаксации артерий по сравнению с контрольными животными. Доксорубицин не оказывал влияния на эффективность опосредованных простагландинами и Ca2+-активируемыми К+-каналами промежуточной и малой проводимости механизмов эндотелийзависимой вазодилатации.

https://doi.org/10.31857/S0869813922110036
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