Зміни біофізичних та морфологічних властивостей міокарда при ожирінні

Ожиріння і артеріальна гіпертензія потенціюють одне одного стосовно до розвитку несприятливого впливу на структуру і функцію серця, збільшується рівень перед- і постнавантаження на серце. Нами проводилось моделювання ожиріння за стандартною методикою висококалорійного харчування, протягом місяця. Вага щурів становить 390-420 гр. На гістологічних зрізах виражений стаз еритроцитів у просвітах капілярів з одиничними дрібними периваскулярними крововиливами, осередкові явища внутрішньосудинного гемолізу, помірно виражене фибриноидное набухання стінок судин. Дифузний набряк строми. Помірно виражена зерниста дистрофія кардіоміоцитів. На гістологічних зрізах брижі кишечнику, у просвітах судин спостерігається виражений стаз еритроцитів, осередкові явища внутрішньосудинного гемолізу, у стінках судин - разволокнение м'язового шару, набряк. Фрагменти передньої черевної стінки: виражений стаз еритроцитів у просвітах судин, набряк гіподерми. Усі ці патологічні зміни призводять до виникнення артеріальної гіпертензії та серцево — судинної недостатності. Obesity is often an additional and leading risk factor for arterial hypertension. The likelihood of hypertension development in individuals with obesity is 50% higher than that of people with normal body weight. Obesity provokes acceleration of the development of factors that make up the cardiovascular risk in general. In obese individuals, arterial hypertension is found 2.9 times more often than in people with normal body mass. In 80% of men and 61% of women included in the Framingham study, the cause of arterial hypertension was an increase in body weight. WHO experts draw the conclusion that in Western countries 1/3 of patients, on average, suffer from arterial hypertension due to excessive body weight, and in men up to 45 years this figure reaches 60%. Obesity and arterial hypertension potentiate each other in relation to the development of unfavorable effects on the structure and function of the heart; the level of pre- and after-load of the heart increases, especially in people with severe and prolonged (> 15 years) obesity. The risk of left ventricular myocardial hypertrophy (LVMH) formation rises from 5.5% in people with normal body weight up to 29.9% in obese people. Hypertension, when associated with obesity, increases the risk of heart hypertrophy more than 4 times. The problem of overweight is the scourge of our time. Obesity is diagnosed quite often. Therefore, a conservative approach is not always reasonable. Surgical treatments for obesity are rather relevant in turn. Objective: to establish morphological changes in the heart and vessels of the anterior abdominal wall and the small intestinal mucus in case of obesity and to establish their role in the occurrence of arterial hypertension. Materials and methods: obesity was modeled according to the standard method of high-calorie nutrition for a month. The weight of rats was 390-420 g. Results and Discussion: the changes in the heart and blood vessels in different areas developed as a result of obesity were examined. The samples of the heart walls are presented in all the layers – the epicardium, myocardium, and endocardium. The endocardium is of usual histological structure, represented by endothelial lining in the form of single layer flat epithelium and such underlying layers – loose connective tissue, muscular and elastic layer, and external connective tissue layer. On the longitudinal sections, cardiomyocytes are represented by cells of elongated rectangular shape with eosinophilic cytoplasm, rounded or oval nuclei, located centrally and paracentrally. The layers of loose connective tissue and vessels are located between the muscular elements of the myocardium. Diffusely located small eosinophilic grains in the cytoplasm of separate groups of cardiomyocytes are present (phenomena of granular myocardial dystrophy). The interstitial stroma is in moderate edema. The plethora of all the vessels of the myocardium (arteries, veins, microvasculature) is noticed and accompanied by erythrostasis phenomena; individual red blood cells are destroyed with the release of brown pigment in the lumen of the vessel. The walls of the vessels are swelled in some places, and the release of red blood cells from the vascular bed is marked around some of them. The anterior abdominal wall is represented by epidermis, dermis, underlying fatty tissue, and muscle layer. In the lumen of the vessels erythrostasis is manifested significantly. The mesentery is represented by the adipose tissue of a usual histological structure with regional lymph nodes. Vessels are full-blooded, in some places defibration and swelling of the muscular layer are present. Conclusions: As it is evident from the histological sections, the reaction of all the parts of the cardiovascular system is expressed in pathological changes that subsequently lead to arterial hypertension and cardiovascular insufficiency