Ограничение ишемического и реперфузионного повреждения миокарда с помощью пре- и посткондиционирования: молекулярные механизмы и мишени для фармакотерапии

Авторы: Е. В. Шляхто, Е. М. Нифонтов, М. М. Галагудза

Организация:
Санкт-Петербургский государственный медицинский университет им. акад. И. П. Павлова; ФГУ «Федеральный центр сердца, крови и эндокринологии им. В. А. Алмазова»

Раздел: Актуальные вопросы кардиологии и смежных дисциплин

Библиографическая ссылка: Креативная кардиология. 2007; (): -

Цитировать как: Е. В. Шляхто, Е. М. Нифонтов, М. М. Галагудза. Ограничение ишемического и реперфузионного повреждения миокарда с помощью пре- и посткондиционирования: молекулярные механизмы и мишени для фармакотерапии. Креативная кардиология. 2007; (): -. DOI:

Ключевые слова: сердце, ишемия, реперфузия, размер инфаркта, кардиопротекция, прекондиционирование, посткондиционирование

Полнотекстовая версия:  

Аннотация

Ограничение размера инфаркта, формирующегося вследствие острой ишемии миокарда, и ослабление таких проявлений ишемического/реперфузионного повреждения миокарда, как станнирование, нарушения ритма и невосстановление кровотока, являются важными задачами современной кардиологии. Прекондиционирование (ПреК) миокарда - один из наиболее эффективных механизмов эндогенной кардиопротекции. Обычно под ПреК понимают повышение устойчивости миокарда к продолжительной ишемии, возникающее после короткого(их) эпизода(ов) ишемии-реперфузии. В настоящее время становится очевидно, что ПреК может быть вызвано целым рядом факторов, оказывающих слабое повреждающее действие на миокард или на организм в целом. В последние годы был разработан новый подход к защите миокарда от реперфузионного повреждения, получивший название ишемического посткондиционирования (ПостК). В настоящем обзоре на основании собственных и литературных данных проводится сравнительная характеристика ПреК и ПостК, а также обсуждаются различные стимулы, вызывающие ПреК. Особое внимание уделяется фармакологическим триггерам ПреК. Кроме того, дается критический анализ клеточных и молекулярных механизмов, лежащих в основе ПреК и ПостК; приводятся данные о возможных путях использования ПреК и ПостК в клинической практике, в частности в кардиохирургии. Дальнейшие исследования будут способствовать созданию фармакологических миметиков ПреК и ПостК, индуцирующих воспроизводимый и стабильный кардиопротективный ответ и в то же время лишенных серьезных побочных эффектов.

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