Abstract
Introduction. Insulin therapy used during acute myocardial infarction (AMI) is associated with a high risk of hypoglycemia and high glycemic variability. Therefore, the search for optimal therapeutic approaches which affect both cardioprotection and glycemic correction is relevant. It is known that agonists of glucagon-like peptide-1 (aGLP1) exhibit a protective effect on the myocardium and are involved in the normalization of carbohydrate metabolism. The combined use of аGLP1 exenatide and insulin can be more effective and safe but not insufficiently studied.The aim of this study was the comparative investigation of the effect of exenatide, insulin, and their combination on the volume of myocardial damage and the level of glycemia in the myocardial ischemia/reperfusion (I/RP) model in rats with experimental diabetes mellitus (DM2).Materials and methods. Neonatal streptozotocin diabetes was modeled in male Wistar rats on the 4th–5th day of life. At the age of 3 months, I/RP was fulfilled in animals with confirmed hyperglycemia. Experimental groups were formed depending on the time of therapy with insulin, exenatide, or their combination; before or after ischemia. Ischemia lasted for 40 min, while reperfusion was 120 min. The size of the myocardium necrosis zone and the changes in glycemia level and its variability were determined.Results. Insulin reduced glycemia, but it increased glycemic variability by 60 % and caused hypoglycemia in 32–37 % of animals. Exenatide reduced blood glucose concentration to the level of fasting glycemia and glycemic variability by 1.5–2 times compared with insulin. Exenatide given before ischemia reduced the area of necrosis by 2.2 times. The combined use of insulin and exenatide was accompanied by the absence of hypoglycemia and a decrease in the necrosis zone by 3.2 times compared to the control.Conclusion. The combined use of aGLP1exenatide and insulin in experimental conditions of I/RP+DM2 is the most effective and safe. This makes promising their joint use in patients with DM2, both at high risk of AMI and those undergoing AMI.
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