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   <ref-type name="Journal Article">17</ref-type>
   <contributors>
    <authors>
     <author>Valentin V. Kataev</author>
     <author>Valentina N. Perfilova</author>
     <author>Igor I. Prokofiev</author>
     <author>Alla A. Nesterova</author>
     <author>Yulia K. Isaeva</author>
     <author>Margarita V. Kustova</author>
     <author>Ivan N. Turenkov</author>
     <author>Anatoly K. Brel</author>
     <author>Kataev, V.A.</author>
    </authors>
   </contributors>
   <titles>
    <title>Cardioprotective effect of hydroxybenzoic acid ester containing neuroactive acid, compound F-26, in conditions of isoproterenol heart failure in rats</title>
   </titles>
   <keywords>
    <keyword>chronic heart failure</keyword>
    <keyword>mitochondrial dysfunction</keyword>
    <keyword>oxidative stress</keyword>
    <keyword>hydroxybenzoic acid derivatives</keyword>
    <keyword>morphometric parameters of&#13;
cardiomyocytes</keyword>
    <keyword>compound F-26</keyword>
    <keyword>mildronate</keyword>
    <keyword>Scopus</keyword>
    <keyword>ВАК</keyword>
    <keyword>Белый список</keyword>
   </keywords>
   <dates>
    <year>2025</year>
    <pub-dates>
     <date>2026-05-18</date>
    </pub-dates>
   </dates>
   <doi>DOI 10.18413/rrpharmacology.11.811</doi>
   <journal>RESEARCH RESULTS IN PHARMACOLOGY</journal>
   <abstract>Introduction: Chronic heart failure (CHF) is a leading public health problem. Its most common&#13;
manifestation is decreased cardiac inotropic reserve. Mitochondrial dysfunction and oxidative stress&#13;
contribute to the progression of CHF. Hydroxybenzoic acid derivatives limit mitochondrial&#13;
dysfunction and oxidative stress, thereby reducing their damaging effects on the heart.&#13;
Materials and Methods: Chronic heart failure (CHF) was modeled by intraperitoneal&#13;
administration of L-isoproterenol to male Wistar rats at a dose of 2.5 mg twice daily for 21 days.&#13;
Four groups of 14 animals each were formed: intact animals, a control group with CHF that&#13;
received saline solution, and experimental animals with CHF that received compound F-26 at a&#13;
dose of 7.9 mg/kg and mildronate –50 mg/kg intraperitoneally once daily throughout the CHF&#13;
simulation period. Cardiac inotropic function was assessed using functional tests: volume&#13;
loading, adrenergic receptor activation, and occlusion of the ascending aorta. Mitochondrial&#13;
oxygen uptake was determined using polarography. Myocardial morphometric analysis was&#13;
performed using micrographs.&#13;
Results and Discussion: Compound F-26 has a positive effect on cardiac inotropic reserves, as&#13;
evidenced by increases in myocardial contraction and relaxation rates, left ventricular pressure,&#13;
and maximum structural activity intensity (MSI) during functional tests. Compound F-26&#13;
improves mitochondrial respiration, reduces MDA concentration, increases SOD activity, and&#13;
has a positive effect on the cross-sectional area, thickness, and volume fraction of&#13;
cardiomyocytes and interstitium.&#13;
Conclusion: Compound F-26 improves cardiac inotropic function, mitochondrial function, the&#13;
antioxidant system of cardiomyocytes, and morphometric parameters.</abstract>
   <urls>
    <web-urls>
     <url>https://repo.bashgmu.ru/publication/5346</url>
    </web-urls>
    <pdf-urls>
     <url>https://repo.bashgmu.ru/files/5539</url>
    </pdf-urls>
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