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   <ref-type name="Journal Article">17</ref-type>
   <contributors>
    <authors>
     <author>Закирова, А.Н.</author>
     <author>Гарифуллин, Б.Н.</author>
     <author>Закирова, Н.Э.</author>
     <author></author>
     <author></author>
    </authors>
   </contributors>
   <titles>
    <title>РОЛЬ КАРВЕДИЛОЛА В ПРЕДОТВРАЩЕНИИ АПОПТОЗА КАРДИОМИОЦИТОВ ПРИ ОСТРОМ ИНФАРКТЕ МИОКАРДА</title>
   </titles>
   <dates>
    <year>2017</year>
    <pub-dates>
     <date>2018-03-12</date>
    </pub-dates>
   </dates>
   <doi>10.20996/1819-6446-2017-13-6-880-884</doi>
   <abstract>Data on the mechanisms of cardiomyocyte apoptosis in myocardial infarction are presented. It has been experimentally established that the ratio of&#13;
the number of cardiomyocytes with signs of apoptosis and necrosis is 30:1 already 2 hours after acute artery occlusion. This fact points out the leading&#13;
role of apoptosis in cardiomyocyte death in acute period of myocardial infarction. Cardiomyocyte apoptosis makes a significant contribution in&#13;
myocardial remodeling and left ventricular dysfunction after myocardial infarction. The essential role of active forms of oxygen in the development&#13;
of cell apoptosis after reperfusion was proved in experimental data. Carvedilol is a third-generation beta-blocker with additional pleiotropic and antioxidant&#13;
effects. The multifactorial positive influence of carvedilol on apoptosis prevention gives the opportunity to adopt experimental results into&#13;
real-life clinical practice. It was established in vivo that administration of carvedilol just after start of coronary reperfusion decreases by 77% the number&#13;
of cells suffered from apoptosis. Carvedilol has antioxidant effects and prevents cell apoptosis due to reduction in calcium concentration in mitochondrial&#13;
matrix. The experimental results and the data of large randomized clinical trials give an opportunity of using carvedilol in treatment of&#13;
myocardial infarction to decrease necrotic zone and prevent cardiomyocyte apoptosis.</abstract>
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     <url>https://repo.bashgmu.ru/publication/1004</url>
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     <url>https://repo.bashgmu.ru/files/1138</url>
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