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Концептуальные и детальные математические модели электрической активности миокарда

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Впервые создана детальная математическая модель клеток синоатриального узла кролика, включающая: подробную расшифровку основных мембранных токов в клетках СУ, функциональные различия клеток истинных и латентных водителей ритма, изменения в клетках при воздействии АЦХ, изменения внутриклеточных концентраций ионов натрия, калия и кальция, функцию саркоплазматического ретикулума.. Показано, что… Читать ещё >

Содержание

  • Список основных терминов и сокращений, использованных в данной работе
  • Обозначения мембранных ионных токов
  • Геометрия клетки
  • Концентрации ионов
  • Равновесные (реверсные) потенциалы
  • Внутриклеточная динамика кальция
  • Буферизация ионов кальция

Концептуальные и детальные математические модели электрической активности миокарда (реферат, курсовая, диплом, контрольная)

Актуальность темы

11.

Цель и задачи исследования

14.

Научная новизна.15.

Научно-практическое значение.16.

Апробация работы.17.

Структура работы.17.

Основные результаты и выводы.

1. Создана простая двухкомпонентная модель миокарда, адекватно воспроизводящая форму потенциала действия и свойство реституции миокарда.

2. Показано, что на границе неоднородности, имитирующей инфарктную зону, образуется трёхмерное реентри типа «вихревое кольцо» с ограниченным временем жизни.

3. Экспериментально и теоретически исследовано взаимодействие и определены траектории взаимодействующих вихрей на больших расстояниях и в случае квадрупольного реентри.

4. Экспериментально и теоретически показано, что на границе уязвимой зоны единичное раздражение вызывает несколько откликовпредсказаны и экспериментально обнаружены затухающие волны во время переходного процесса.

5. Впервые создана детальная математическая модель клеток синоатриального узла кролика, включающая: подробную расшифровку основных мембранных токов в клетках СУ, функциональные различия клеток истинных и латентных водителей ритма, изменения в клетках при воздействии АЦХ, изменения внутриклеточных концентраций ионов натрия, калия и кальция, функцию саркоплазматического ретикулума. .

6. При моделировании обнаружен и исследован ранее неизвестный режим прекращения спонтанной активности без предварительного замедления ритма и немонотонная зависимость порога возбуждения от концентрации АЦХ.

7. Показано, что преавтоматическая пауза в синоатриальном узле при отсутствии АЦХ составляет лишь 0.4 с, а в присутствии АЦХ может длиться десятки секунд. Выявлен механизм формирования паузы, основанный на сдвиге ионного гомеостаза под действием АЦХ и высокочастотной стимуляции.

8. Показано, что флуктуации мембранного потенциала возрастают с увеличением концентрации АЦХ и наиболее заметны на границе потери спонтанной активности.

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