Гиперхолестеринемия атеросклероз. Атеросклероз

Примечание: Р - достоверность различий показателей в сравнении с контрольной группой до лечения; P1 - достоверность различий показателей в сравнении с контрольной группой после лечения; Р2 - достоверность различий показателей по группам до и после лечения.

Гликирование липопротеидов нередко сопровождается и их окислением (переоксидацией). В этом случае процесс назьвают гликооксидацией. Липопротеиды, которые подвергаются гликооксидации, оказывают выраженное атерогенное воздействие [79].
У больных СД гликирование ЛПНП может сочетаться с их десиалированием, вызывая более глубокое изменение липидного состава [81]. Это свидетельствует о том, что атерогенность ЛПНП может быть обусловлена их несколькими модификациями [80]. Наряду с развитием дислипидемий постоянная (хроническая) гиперинсулинемия (экзогенная при СД I и эндогенная при СД II типа) оказывает стимулирующее воздействие на пролиферацию гладкомышечных клеток сосудистой стенки., способствуя прогрессированию атеросклероза [78]. Инсулин действует как атерогенный гормон в дозах, превышающих физиологические, например при инсулинорезистетности. Небольшие дозы инсулина наоборот могут оказывать антиатерогенное действие, способствуя образованию оксида азота, эндотелиального фактора релаксации [82]. Нами изучено состояние липидного обмена у больных ИБС, СД II типа, у группы здоровых лиц и больных ИБС, страдающих СД II типа. Как видно из приведенной таблицы у больных ИБС, СД II типа и при их сочетании наблюдаются сходные изменения. Они характеризуются увеличением уровня общего холестерина по сравнению с контрольной группой, значимым снижением уровня липопротеидов высокой плотности (ЛПВП) гипертриглицеридемией (Р<0.05). Обращает на себя внимание увеличение уровня липопротеидов низкой плотности и липопротеидов очень низкой плотности и значимо более высокое значение коэффициента атерогенностн. Таким образом, к особенностям нарушений липидного обмена у больных, страдающих СД II и ИБС можно отнести наличие гиперхолестеринемии, гипертриглицеридемии, снижение уровня ЛПВП, повышение уровня ЛПНП и ЛПОНП. Указанные нарушения способствуют развитию и прогрессированию коронарного атеросклероза. Полученные нами данные согласуются с результатами исследований других авторов.


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