Publications by authors named "E V Lukoshkova"

The cardiohemodynamics was studied 1 week after the administration of streptozotocin (60 mg / kg) or 2 weeks after a dose of 30 mg / kg. All rats had a significantly elevated level of glucose in the blood (up to 27-31 mM). In an echocardiographic study, about 1/3 of diabetic animals exhibited systolic dysfunction, and the remaining 2/3 - diastolic dysfunction with an increase in isovolumic relaxation time by 1.

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Aim      To study left ventricular (LV) hemodynamics in presence of decreased blood inflow to the heart as well as changes in myocardial content of energy metabolites in diabetic rats.Material and methods  Diabetic cardiomyopathy is characterized by impaired heart contractility and by transition of cardiomyocyte energy metabolism fatty acids exclusively as a source of energy. This reduces the efficiency of energy utilization and increases the heart vulnerability to hypoxia.

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Nitric oxide (NO) has been shown to stimulate differentiation and increase the survival of ganglionic sympathetic neurons. The proportion of neuronal NOS-immunoreactive sympathetic preganglionic neurons is particularly high in newborn rats and decreases with maturation. However, the role of NO in the development of vascular sympathetic innervation has never been studied before.

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Impaired insulin synthesis is accompanied by hyperglycemia and the development of diabetic cardiomyopathy. Echocardiography and left-ventricular catheterization were employed for studying the contractile function of the left ventricle in 2 weeks after administration of streptozotocin (60 mg/kg). The results obtained by both methods were similar and indicated the development of systolic dysfunction with a 27% decrease in cardiac output.

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This work was designed to study changes in the mechanical properties of rat myocardium during short-term (2-3 sec) compression of the lower vena cava. A catheter was inserted into the left ventricle, allowing simultaneous measurement of left-ventricular volume and pressure. The decrease in the left-ventricular end-diastolic volume caused by inflow restriction was accompanied by less pronounced decrease in the left-ventricular stroke volume and maximum rate of left-ventricular pressure development.

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