Hyperleptinemia Results in Systemic Inflammation and the Exacerbation of Ischemia-Reperfusion Myocardial Injury: The Involvement of the JAK/STAT Pathway

Abstract

Hyperleptinemia potentiates the effects of many atherogenic factors, such as inflammation, platelet aggregation, migration, hypertrophy, proliferation of vascular smooth muscle cells, and endothelial cell dysfunction. The present study analysed the effects of long-term hyperleptinemia in an in vivo myocardial ischemia-reperfusion model to demonstrate whether the in vivo deleterious effect also affects cardiac structure and function. Rats by were subcutaneously administered leptin for 8 days to estimate the involvement of the JAK/STAT pathway. Data from 58 male Wistar rats were included in the final analysis. Myocardial infarction (MI) was modelled by the 30-minute ligation of the main left coronary artery followed by 120-minute reperfusion. Hemodynamic measurements, electrocardiography monitoring, echocardiography, myocardial infarct size and area at risk, blood biochemical parameters, leptin, IL-6, TNF-alpha, FGF-21, and cardiomyocyte morphology were measured. Statistical analyses were performed using IBM SPSS Statistics v.26. Seven-day hyperleptinemia in rats led to increased an blood pressure and heart rate, myocardial hypertrophy, impaired LV function, an increased frequency of ischemic arrhythmias, dyslipidaemia, systemic inflammation, and an increased size of induced myocardial infarction. The blockade of the JAK/STAT signalling pathway effectively reversed the negative effects of leptin, including increased blood pressure and total cholesterol.

The first experience of the combined use of nitric oxide and molecular hydrogen for cardiac surgery in high-risk patients

“…Тем не менее до сих пор сохраняется проблема интраоперационного ишемическиреперфу зионного повреждения миокарда (ИРПМ), актуальная вследствие определяющего влияния на клиническое течение раннего послеоперационного периода. Имен но интраоперационное повреждение миокарда (ПМ) в первую очередь определяет развитие острой сер дечной недостаточности (ОСН) после 15-20 % вме шательств на сердце и нарушений ритма после 30 % этих процедур [1][2][3].…”

“…The first experience of the combined use of nitric oxide and molecular hydrogen for cardiac surgery in high-risk patients Vladimir V. Pichugin 1  , Anna V. Deryugina 2 , Stepan E. Domnin 1 , Alexander S. Shirshin 3 , Sergey A. Fedorov 1 , Sergey N. Buranov 3 , Sergey A. Jourko 1 , Michail V. Ryazanov 1 , Yuriy D. Brichkin 1 , Darya A. Danilova 2 Пичугин В.В. и др.…”