kpcczКомплексные проблемы сердечно-сосудистых заболеванийComplex Issues of Cardiovascular Diseases2306-12782587-9537Federal State Budgetary Institution “Research Institute for Complex Issues of Cardiovascular Diseases”10.17802/2306-1278-2015-3-37-46kpccz-138Research ArticleФУНДАМЕНТАЛЬНЫЕ АСПЕКТЫ БОЛЕЗНЕЙ ОРГАНОВ КРОВООБРАЩЕНИЯFUNDAMENTAL ISSUES IN CIRCULATORY SYSTEM DISEASESИШЕМИЧЕСКОЕ ПОСТКОНДИЦИОНИРОВАНИЕ СЕРДЦА. АНАЛИЗ ЭКСПЕРИМЕНТАЛЬНЫХ И КЛИНИЧЕСКИХ ДАННЫХISCHEMIC POSTCONDITIONING OF HEART. ANALYSIS OF EXPERIMENTAL AND CLINICAL DATAМасловЛеонид НиколаевичMaslovLeonid N.

634012, г. Томск, ул. Киевская, д. 111А

111A, Kievskaya st., Tomsk, 634012

Maslov@cardio-tomsk.ruХалиулинИ. Г.KhaliulinI. G.

Бристоль

Bristol

Федеральное государственное бюджетное научное учреждение «Научно-исследовательский институт кардиологии»РоссияFederal State Budgetary Scientific Research Institute for CardiologyRussian FederationУниверситет БристоляВеликобританияUniversity of BristolUnited Kingdom201524112015033746Copyright © Маслов Л.Н., Халиулин И.Г., 20152015Маслов Л.Н., Халиулин И.Г.Maslov L.N., Khaliulin I.G.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.nii-kpssz.com/jour/article/view/138

Литературные данные о влиянии экспериментального атеросклероза на инфаркт-лимитирующий эффект ишемического посткондиционирования (ИПост) носят противоречивый характер. Представленные данные свидетельствуют о том, что старение устраняет или ослабляет инфаркт-лимитирующий эффект посткондиционирования, но не влияет на антиаритмический эффект ИПост. Большинство экспериментальных данных сообщают о том, что стрептозотоцин-индуцированный диабет устраняет инфаркт- лимитирующий эффект ИПост. Относительно сахарного диабета 2-го типа сведения носят противоречивый характер: одни авторы утверждают, что подобный диабет полностью нивелирует кардиопротекторный эффект ИПост, другие говорят о том, что он только ослабляет, но не устраняет инфаркт-лимитирующий эффект ИПост. Посткондиционирование у крыс с повышенным артериальным давлением предупреждает появление реперфузионной сократительной дисфункции сердца и оказывает инфаркт-лимитирующий эффект. Гипертрофия сердца, постинфарктное ремоделирование и дилатационная кардиомиопатия не влияют на инфаркт-лимитирующий и инотропный эффект посткондиционирования. Согласно большинству публикаций, ИПост усиливает инотропный и кардиопротекторный эффект кардиоплегии. Данные о влиянии посткондиционирования на толерантность сердца человека к действию ишемии-реперфузии носят ограниченный характер и не позволяют сделать однозначный вывод о том, может ли ИПост предупреждать реперфузионные повреждения миокарда у кардиологических пациентов.

Published data on the impact of the experimental atherosclerosis on the infarct-limiting effect of ischemic postconditioning (IPost) are controversial. The reviewed data indicate that aging eliminates or reduces the infarct-limiting effect of postconditioning but does not affect the antiarrhythmic effect of IPost. Most of the experimental data reported that streptozotocin-induced diabetes removes the infarct-limiting effect of IPost. Regarding the second type of diabetes, information is contradictory: some authors argue that this diabetes completely eliminates the cardioprotective effect of IPost, others say that it only weakens but does not eliminate the infarct-limiting effect of IPost. Postconditioning in rats with high blood pressure prevents the appearance of reperfusion contractile dysfunction of the heart and provides the infarct-limiting effect. Cardiac hypertrophy, post-infarction remodeling and dilated cardiomyopathy have no effect on the infarct-reducing and inotropic effect of postconditioning. The majority of publications indicates that IPost enhances the inotropic and cardioprotective effect of cardioplegia. Data on the effect of postconditioning on the tolerance of the human heart to ischemia/reperfusion are limited and do not allow to make an unambiguous conclusion about whether IPost prevents reperfusion myocardial injury in cardiac patients.

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The authors declare that there are no conflicts of interest present.