Vіsnik Naukovih Doslіdžen' (Nov 2017)
METABOLIC AND STRUCTURAL MYOCARDIAL DISEASE IN THE CONDITIONS OF EXPERIMENTAL ACUTE LUNG INJURY
Abstract
The study of metabolic and structural myocardial disorders in conditions of experimental acute lung injury allows revealing the pathogenesis of processes and predicting the peculiarities of the course in this pathology. The aim of the study – to find out the dynamic indicators of peroxide lipid oxidation, antioxidant protection and pathomorphological changes in the heart under conditions of experimental state lung injury. Materials and Methods. Experiments were conducted on white nonlinear male-rats weighing 200–220 g. Modeling of acute lung injury was performed according to the method of G.Matute-Bello. Animals were excised from the experiment at 12, 24, 48 and 72 hours after the simulation of acute lung injury. To study morphological changes, myocardial biopsies were used, the sections of which were stained with hematoxylin and eosin. In the heart homogenate established indicators of lipid peroxidation and antioxidant protection. Results and Discussion. In the acute lung injury due to intracutaneous administration of chloride acid, the processes of lipid peroxidation are activated in the heart, as evidenced by the accumulation of TBA-active products of the LPO, with a maximum of 24 hours (by 74.7 % compared with the control, p <0.05). Under these conditions, the indexes of the enzymatic level of antioxidant defense with a compensatory increase above the control level of SOD in 48 hours (by 88.3 %, p <0.05), catalase after 72 hours (by 63.5 %, p <0.05). Under the conditions of modeling of acute lung injury, the structure of myocardial damage with uneven blood filling of blood vessels in 12 hours of observation, the formation of cellular infiltrates of stroma in 24 hours, an increase in paresis phenomena, erythrostasis, stroke edema, focal dystrophic changes in cardiomyocytes, small focal cell infiltration after 48 hours, appearance erythro- and plasmapostasis, deepening of edema, fragmentation of fibers and their focal wave-like deformation after 72 hours. Conclusions. The given data testify to the systemic pathogenic effect of acute lung injury on the organism of experimental animals, in particular on the heart with a maximum of metabolic disturbances in 24 hours and the activation of compensation mechanisms in 48–72 hours.
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