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Alcohol is one of the leading causes of death worldwide, annually taking 3 million lives. Alcohol abuse to a greater degree negatively affects the functioning of the cardiovascular system. Aim. Studying the severity of pathomorphological changes in the heart of deceased patients with alcoholism. Materials and methods. The heart sections of 35 deceased alcoholic patients (38–60 years old) were taken for histo-morphometric analysis. As a comparison group, the material of deceased patients (n = 15), suffering from ischemic heart disease (IHD) and hypertension disease (HD) was studied. Results. In conditions of alcoholism in 100 % of cases myocardium showed marked microcirculatory disorders, increased vascular permeability. In all cases sclerotic changes similar in topography to the comparison group were noted, however, sclerosis of large arterioles was 1.9 times less pronounced than in IHD group. In the myocardium of alcoholics, edema, atrophy of cardiomyocytes bundles and areas of fatty stroma are common. In 20 % of cases, there were mosaic necrosis of individual cardiomyocytes and small focal necrosis of small groups of cells, fibrinoid necrosis of small branches of coronary arteries. Compared with IHD group the number of fatty degenerated cardiomyocytes increased by 1.23 times, fuchsinophilic cardiomyocytes – by 1.38 times with simultaneous reducing severity of sclerotic changes in vessels by 1.9 times. Sclerotic changes in stroma are significantly higher in relation to IHD and HD groups (by 1.88 and 6.94 times, respectively). Conclusions. The morphogenesis of heart damage during alcoholism consists of combination of dystrophic, necrotic, atrophic and sclerotic changes – morphological substrate of alcoholic cardiomyopathy. These signs, based on quantitative analysis, are important criteria necessary for the thanatogenetic analysis in cases of death on the background of alcoholism.

The aim of the study. To study the pathomorphological changes of the vascular bed and the state of collateral blood flow in cerebral infarction. Materials and methods. The brains of 45 deceased patients with hemispheric infarctions with different terms of the disease were studied during the work. The comparison group consisted of 10 patients who died suddenly from acute coronary insufficiency, who did not have diseases of the nervous system. To assess the morpho-functional state of blood vessels and the intensity of blood flow the cross-sectional area of blood vessels, the area of endothelial cell nuclei, the density of their location and the length of the capillary network were determined. Results. In the early stages of stroke, along with the processes of irreversible damage of small capillaries in the area of infarction and partly in the area of the penumbra, myocardial thrombosis and constant number of vessels in the perifocal area of infarction, there are processes aimed at providing effective blood flow in ischemic areas of brain by increasing collateral blood flow from the leptomeningeal vessels, increasing the diameter of blood vessels and the length of the capillary network. On the 6th day of the disease, the processes of collagenization of the subarachnoid space are registered, which reduced the collateral blood flow from the pial vessels to the underlying cortical parts of the brain. With the increasing of the disease duration, the diameter of the capillaries returns to initial values, in the perifocal areas of the infarct there is a recalibration of the lumen of the arterioles with a decrease in the total cross-sectional area of newly formed vessels, a significant number of arterioles with obliteration of the lumen are present. Conclusions. In the early stages of ischemic stroke there is an increase in blood circulation due to an increase in the diameter of the capillaries, the length of the capillary network and increased collateral circulation by the pial vessels. In the long-term period there is a reduction in the total area of the lumen of arterioles and a decrease in the efficiency of collateral blood flow, which should be regarded as an adaptive response of the vascular bed to decreased need for blood supply to stroke areas at the stage of cyst formation.

У статті висвітлені питання викладання клінічної патогістології для лікарів-лаборантів у відповідності до затвердженої програми з навчальної дисципліни. Підкреслена роль клінічної патогістології в прижиттєвій діагностиці значної кількості патологічних процесів, що вкрай необхідно при підготовці фахівців з діагностичної медицини.