The efficiency of remote ischemic postconditioning of the myocardium in rats with induced metabolic syndrome depends on the leptin level

Abstract

Remote postconditioning (RPost) has a great therapeutic potential for protecting the myocardium during ischemiareperfusion in clinical practice. At the same time, an important problem limiting the use of conditioning effects in the clinic is the presence of metabolic disorders in the patient. The aim of this work was to assess the effect of induced metabolic syndrome (iMetS) on the efficacy of the infarct-limiting effect of remote ischemic postconditioning (RPost) in rats and to study the mechanisms of this effect.The study was carried out on Wistar rats. MetS was induced by high-carbohydrate high-fat diet. Criteria of metabolic syndrome were an increase in the weight of animals, abdominal fat volume, the development of arterial hypertension, hypercholesterolemia, an increase in triglycerides in serum, hyperleptinemia, hyperglycemia, the development of a state of insulin resistance by a significant increase in the Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) index and glucose tolerance. All animals were subjected to 45 min coronary occlusion and 120 min reperfusion.RPost led to a twofold reduction of infarct size in rats with intact metabolism (р < 0.0001), while in rats with iMetS a decrease in infarct size during RPost was 25 % (p = 0.00003), which was significantly lower than in animals without iMetC (р < 0.0001). A direct correlation was found between of infarct size during RPost and the serum leptin level of rats with iMetC.The presented data suggested that a decrease in the efficiency of remote postconditioning in rats with diet-induced metabolic syndrome depends on leptin content in blood.

The Signaling Mechanism of Remote Postconditioning of the Heart: Prospects of the Use of Remote Postconditioning for the Treatment of Acute Myocardial Infarction

“…We tried evaluating the role of the autonomic nervous system in RPost. Rats were subjected to CAO (45 min) and reperfusion (2 h) [ 20 ]. RPost was induced by the repeated I/R of hindlimbs.…”

“…We found that blocking peripheral opioid receptors completely abolished the infarct-reducing effect of RPost induced by hind limb I/R in rats [ 20 ]. It was detected that opioid peptide deltorphin II can mimic RPost [ 30 , 31 ].…”

“…RPost was induced by three cycles of bilateral hindlimb ischemia (5 min) and reperfusion (5 min). RPost limited infarct size by 50% [ 20 ]. We found that the KATP channel blocker glibenclamide completely reversed the infarct-sparing effect of RPost [ 20 ].…”

“…RPost limited infarct size by 50% [ 20 ]. We found that the KATP channel blocker glibenclamide completely reversed the infarct-sparing effect of RPost [ 20 ]. The MPT pore opener atractyloside also abolished the infarct-reducing effect of RPost [ 20 ].…”

Development of cardioprotective effect of chronic continuous hypoxia in rats with induced metabolic syndrome

“…В данном исследовании мы не обнаружили стати стически значимого снижения размера инфаркта мио карда у крыс с МетС. Это согласуется с данными, полу ченными в экспериментах на самцах крыс Вистар, по лучавших ВУВЖД, аналогичную используемой в данном исследовании [9]. T. Thim и соавт.…”