Morphological Changes in Heart Tissue When Exposed to Pulsed Currents in Chronic Purulent Pneumonia (Experimental Study)

A model of experimental chronic purulent pneumonia was induced in mongrel white rats. Morphological changes in the heart tissue were manifested by uneven hypertrophy of cardiomyocytes, thickening of vascular walls and increasing their quantitative ratio, moderate growth of connective tissue layers in perivascular zones, intermuscular edema with impaired blood circulation of the muscle wall. When electromyostimulation with pulsed currents of respiratory muscles in the heart tissue revealed dystrophic swelling and focal dilution of cardiomyocytes, uneven inter-daily edema, hypertrophy of the walls of arterioles, full blood, circulatory disorders in the form of focal hemorrhages in the myocardium and epicardium. Chronic Obstructive Pulmonary Disease (COPD) is considered as one of leading diseases of morbidity among the population of the world. The disease progresses rapidly, leading to early disability of patients, thereby causing significant economic and social damage [1]. Due to pneumonia, the cardiovascular system stops functioning properly, worsening the prognosis of recovery. Pathomorphological changes in the heart with COPD and pulmonary hypertension are characterized mainly by 2 types of changes. For the first (hypertrophic-hyperplastic) type is characterized not so much by dilatation as by hypertrophy of the right ventricle of the heart. In the second type of restructuring, there is a combination of myogenic dilatation of the right ventricle with myocardial hypertrophy and, less commonly, with expansion of the left ventricle cavity. Atrophic-sclerotic processes predominate in the muscle fibres of the right ventricle. The endocardia fibroelastosis is expressed in the right atrium and right ventricle. The muscle fibres in the left ventricle are not changed or predominate their hypertrophy, and cardiosclerosis has a large-scale character feature and is signed only in the presence of concomitant diseases (arterial hypertension, atherosclerosis) [1]. The major reason of death in COPD is recognized as the development of severe respiratory and pulmonary heart failure [3-7].

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