AIMTo evaluate the effects of glucagon-like peptide-1 analogs (GLP-1a) combined with insulin on myocardial ischemia-reperfusion injury in diabetic rats.METHODSType 2 diabetes mellitus (T2DM) was induced in male Wistar rats with streptozotocin (65 mg/kg) and verified using an oral glucose tolerance test. After anesthesia, the left coronary artery was occluded for 40 min followed by 80 min reperfusion. Blood glucose level was measured during surgery. Rats were randomized into six groups as follows: (1) control rats; (2) insulin (0.1 U/kg) treated rats prior to ischemia; (3) insulin (0.1 U/kg) treated rats at reperfusion; (4) GLP-1a (140 mg/kg) treated rats prior to ischemia; (5) GLP-1a (140 mg/kg) treated rats at reperfusion; and (6) rats treated with GLP-1a (140 mg/kg) prior to ischemia plus insulin (0.1 U/kg) at reperfusion. Myocardial area at risk and infarct size was measured planimetrically using Evans blue and triphenyltetrazolium chloride staining, respectively.RESULTSThere was no significant difference in the myocardial area at risk among groups. Insulin treatment before ischemia resulted in a significant increase in infarct size (34.7% ± 3.4% vs 18.6% ± 3.1% in the control rats, P < 0.05). Post-ischemic administration of insulin or GLP-1a had no effect on infarct size. However, pre-ischemic administration of GLP-1a reduced infarct size to 12% ± 2.2% (P < 0.05). The maximal infarct size reduction was observed in the group treated with GLP-1a prior to ischemia and insulin at reperfusion (8% ± 1.6%, P < 0.05 vs the control and GLP-1a alone treated groups).CONCLUSIONGLP-1a pre-administration results in myocardial infarct size reduction in rats with T2DM. These effects are maximal in rats treated with GLP-1a pre-ischemia plus insulin at reperfusion.
Metoprolol treatment in cardiovascular diseases is discussed considering efficiency, safety and pharmacoeconomic aspects. The article reviews the main clinical trials of metoprolol and its different forms (Extended-Release and Immediate-Release metoprolol, tartrate and succinate).
Background. Percutaneous coronary intervention (PCI) in patients with ischemic heart disease (IHD) is followed often by myocardial injury. Up to now there is no mutual agreement to the infl uence of the perioperative myocardial injury on the long-term prognosis of the IHD patients.Objective. The aim of study was to assess the risk factors for the development of cardiac events in the long-term period in patients with stable coronary artery disease with myocardial damage after PCI.Materials and methods. The study included 113 patients with stable coronary artery disease who underwent planned PCI. Serum troponin levels were determined before and 24 hours after the intervention. Re-examination of patients was carried out after 12–18 months (average 15 months).Results. The post PCI Tn I level over a reference one was registered in 25 patients (22,2 %). During the follow-up period the cardiovascular events took place in 25,6 % patients: acute myocardial infarction (MI) in 3 (2,6 %), angina occurred in 23 %. One-way ANOVA revealed a signifi cant value for cardiac risk events of the patient age, number of stenosed arteries, summary degree of stenosis, and their complicity, number of implanted stents. The fi rst three of them were included in the fi nal combination of the stepwise discriminant analysis. The general linear model of the latter detected additionally statistical signifi cance of the variables “MI in the past” (before PCI) and “number of postdilatations“.Conclusion. In patients with stable ischemic heart disease, included in the study, the determining risk factors for the development of cardiac events were the prevalence and nature of the obstructive lesion of the coronary bed, age, previous myocardial infarction, and especially the performance of PCI. Myocardial damage was not identifi ed as a risk factor for recurrent angina or myocardial infarction.
Norepinephrine, blockers of beta-adrenoreceptors, angiotensin-converting enzyme inhibitors and angiotensin I receptor blocker were investigated in organotypic tissue culture of cardiomyocytes of 10-12-day-old chicken embryos and newborn rat heart in a wide range of concentrations. The data obtained show that low concentration of norepinephrine led to the cardiomyocyte growth control. The application of beta-adrenoblockers metoprolol and atenolol prevented stimulating effect of norepinephrine. Zofenopril inhibited the growth of cardiomyocytes but enalapril had no effect on this process. The effect of angiotensin I receptor blocker depended on concentration - low concentrations resulted in activation of cardiomyocyte growth; and high concentrations led to the decrease of their growth.
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