Role of A2-adrenoceptors in Rat Heart with the Model of Myocardial Infarction

Journal of Chemical Health Risks

دوره 11، شماره 2، شهریور 2021، صفحه 129-134   

نوع مقاله: Original Article

شناسه دیجیتال (DOI): 10.22034/jchr.2021.682031

نویسندگان

Anna Mihailovna Kuptsova^{* 1}؛ Roman Kutdusovich Bugrov²؛ Insaf Ilkhamovich Khabibrakhmano³؛ Roman Sergeevich Kobzarev²؛ Nafisa Ilgizovna Ziyatdinova⁴؛ Timur Lvovich Zefirov⁴

¹Associate Professor (Department of Human Health Protection) Institute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia

²Рostgraduate (Department of Human Health Protection) Institute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia

³Senior Lecturer (Department of Human Health Protection) Institute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia

⁴Professor (Department of Human Health Protection) Institute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia

چکیده

Chronic adrenergic and angiotensin-energic stimulation of the heart muscle is one of the main causes of the onset and development of heart failure. α₂-AR is widespread in the cardiovascular system and can be further applied and introduced into the heart's regenerative cell therapy. This study's objective was to study the effect of α₂-AR stimulation on the performance of an isolated heart in rats with a model of myocardial infarction. To study the mechanisms of MI, experiments were carried out according to the classical technique of H. Selye - ligation of the anterior branch of the left coronary artery and perfusion of a Langendorff heart with a model of myocardial infarction. We studied the parameters of myocardial activity by changes in heart rate, as well as the left ventricle pressure (LVP), and the CF (dp/dt_max)/(dp/dt_min) of the left ventricle. Coronary dilator activity was assessed by measuring the outflow of the perfusion solution through the coronary arteries. The amplitude of the left ventricle's pressure wave after application of the α₂-AR agonist clonidine hydrochloride at a concentration of 10^-6 M to the perfused solution increased by 44% (p≤0.05) from the initial values. The rate of contraction and the rate of relaxation of the left ventricular myocardium also increased by 20% (p≤0.05) and 37% (p≤0.05), respectively. The activation of α2-AR in adult rats' isolated hearts with a model of myocardial infarction caused a decrease in heart rate by 18% (p≤0.05) and CF by 2% (p≤0.05).

کلیدواژه‌ها

Model؛ Myocardial infarction؛ α2-adrenoreceptors؛ Isolated heart؛ Rat

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