[Embryology, anatomy and rare pathologies of the popliteal artery: Peculiarities of surgical treatment]. / Émbriologiia, anatomiia i redkie patologii podkolennoi arterii: osobennosti khirurgicheskogo lecheniia.

Knowledge of anatomical variations of the division of the popliteal artery and specific lesions of the arterial segment involved is necessary for the surgeon, traumatologist-orthopaedist, vascular surgeon. The article contains a review of recent literature data on the prevalence of different variants of branching patterns of the arteries of the crus, also providing a detailed discussion of embryological development of the arterial system of the lower extremities, in many ways explaining the appearance of rare pathologies of the popliteal artery, such as for example popliteal artery entrapment syndrome. Particular attention is paid to cystic damage of the popliteal artery, describing currently known theories of the development of this rare pathology, this is accompanied by sharing own experience in surgical treatment of the patients involved. Awareness of anatomical variants and peculiarities of embryonic development contributes to decreasing the possibility of iatrogenic damage of the popliteal artery during orthopaedic operations and to appropriate decision-making as to the method of revascularization.

[Histochemical characteristics of adrenergic myocardial and adrenal fibers in experimental narrowing of the aorta and pulmonary artery].

Ligation of the aorta or the pulmonary trunk was the method of experimental overloading of heart ventricles. Histochemical studies indicated activation of mediator chain of the sympatho-adrenal system. Catecholamines content in the nervous plexus of the overloaded ventricle did not change but there was an increase of their content in the medullary layer of the adrenals. Thus, chromaffin cells activity increases and desympathization of the heart muscle may be an important step in pathogenesis of heart failure in acute arterial hypertension.

[Morphologic criteria of the adaptation of the vascular bed of the myocardial ventricles in acute massive embolism of the pulmonary arteries in an experiment]. / Morfologicheskie kriterii adaptatsii sosudistogo rusla miokarda zheludochkov pri ostroi massivnoi émbolii legochnykh arterii v éksperimente.

Acute massive pulmonary embolism was induced in 94 random-bred dogs. There were 3 groups of the time control (0, 1 and 6 hrs) and 4 experimental groups (1- and 6-hrs compensated, 1- and 6-hrs decompensated). Favorable signs of the vascular adaptation: moderate arterial plasmorrhagia; lack of blood stasis, heterogeneity of metabolic profiles of arteries; prevalence of anaerobic glycolysis; some prevalence of catabolic reactions over anabolic reactions. Non-favorable signs: considerable plasmorrhagia; perivascular edema; multiple stases and hemorrhages; venous thrombosis; a dramatic decrease of the enzymatic activity in the arterial wall.

[The sympathetic innervation of the myocardium and its damage in acute massive pulmonary embolism]. / Simpaticheskaia innervatsiia miokarda i ego povrezhdenie pri ostroi massivnoi legochnoi émbolii.

The state of the adrenergic heart innervation and injuries of right (RV) and left (LV) ventricles in experimental massive embolism of pulmonary arteries (MEPA) were studied in 62 dogs under conditions of the intact thorax and natural respiration. The degree of focal myocardial injuries depended upon the density of the sympathetic innervation: when the density of adrenergic nerves (AN) was high the number of injuries decreased. Hypercatecholaminemia developing at the early period of MEPA has a cardiotoxic effect, more pronounced in dogs with decompensation. A decrease of the AN density and increase of injuries in RV and LV were observed in long-term experiments. The results allow explaining the possibility of the adaptation processes breakdown by the development of heart failure in acute MEPA.

[The neurohormonal changes in acute pulmonary embolism (clinico-experimental research)]. / Neirogormonal'nye izmeneniia pri ostroi legochnoi émbolii (kliniko-éksperimental'noe issledovanie).

The state of sympathetic-adrenal and adrenocortical systems was studied in experimental massive pulmonary embolism (PE) and also in patients with massive PE or with embolism of pulmonary artery branches. In experimental massive PE the marked stimulation of adrenal medulla cells was due to specific pathophysiological changes. On the contrary, the moderate activation of adrenal cortex cells was due to nonspecific stress factors such as immobilization of the dogs or catheterization of the heart and vessels. The experimental massive PE was characterized by parallel activation of both parts of the sympathetic-adrenal system. A significant rise of cortisol blood concentration was revealed in the patients with massive PE, but not in those with embolism of the pulmonary artery branches or during the first 6 hours of experimental massive PE. Thus, this investigation shows the activation of the sympathetic-adrenal and adrenocortical system during PE and also the dependence of these neurohormonal changes on the volume and duration of embolic occlusion.

[The sympathetic-adrenal system in experimental massive pulmonary embolism]. / Sostoianie simpatiko-adrenalovoi sistemy pri éksperimental'noi massivnoi legochnoi émbolii.

The density of adrenergic nervous plexus in ventricular myocardium, the concentration of catecholamines in blood and in adrenal medulla were studied on 24 dogs with acute massive pulmonary embolism (MPE) and also on 13 control dogs. Moderate and shortterm activation of adrenal system took place in control group. During the first hour of MPE the activation of both adrenal and mediator systems was revealed. To the six hour of MPE the enlarged activity of adrenal chromaffin cells was maintained, but the density of adrenergic nervous plexus in ventricular myocardium decreased. In cases, when MPE was followed by heart failure, a quick and significant decrease of mediator concentration in myocardium and increase of adrenal medullary cells activity took place. Thus, the velocity of revealed changes may be the reason of transition processes exit to compensative or decompensative state.

[Status of the myocardial ventricles in thromboembolism of the pulmonary arteries and their branches (based on early autopsy material)]. / Sostoianie miokarda zheludochkov pri tromboémbolii legochnykh arterii i ikh vetvei (na materiale rannikh vskrytii).

Ventricle myocardium of 16 patients who had died from acute thromboembolism (TE) of the pulmonary arteries was studied. The most important factor in the development of myocardial alterations is the degree of a vascular occlusion by the thrombus. Chronic lung and heart diseases as well as patient age may considerably aggravate the structural changes of the cardiomyocytes. Relatively low activity of catabolic enzymes in the myocardium of patients with TE correlates with a small size of embolic damage, the presence of chronic lung and heart diseases and with advanced age.

[Changes in the dehydrogenase activity of the cardiomyocytes in experimental acute massive pulmonary embolism]. / Izmenenie aktivnosti degidrogenaz kardiomiotsitov pri ostroi massivnoi émbolii legochnoi arterii v éksperimente.

A study of the activity of SDG, LDG, NAD-D in several structures of the heart was carried out in acute compensated massive embolism of the pulmonary artery. TV-histophotometry demonstrated heterogeneity of metabolic processes in the myocardium in the control and experimental group. The animals with pulmonary artery embolism showed diverse hemodynamic changes in the lesser and greater circulation. Loads to right cardiac compartments were accompanied by an elevation of SDG, NAD-D in the interventricular septum.

[Lesions of ventricular cardiomyocytes in experimental massive pulmonary embolism]. / Povrezhdeniia kardiomiotsitov zheludochkov pri éksperimental'noi massivnoi émbolii legochnykh arterii.

The damage of ventricular myocardial cells during acute experimental massive pulmonary embolism (MPE) was studied by light, polarization and electron microscopy on anaesthetized dogs. In cases, when MPE was followed by heart failure, the deep ir reversible damage of myofibrils took place, and the relative volume of myofibrils decreased in both ventricles. The damage of right ventricular myocardium, which works against increased postload during MPE, may be reason of right ventricular insufficiency.

[Clinico-experimental study of histoenzymological changes in the ventricular myocardium in pulmonary embolism]. / Kliniko-éksperimental'noe issledovanie gistoénzimologicheskikh izmenenii v miokarde zheludochkov pri legochnoi émbolii.

The SDH and LDH activity in ventricular myocardium was studied in early autopsies of 16 patients, which died from acute pulmonary thromboembolism, and also in 17 dogs with experimental pulmonary embolism. In general the data of histoenzymological study of experimental and sectional material were identical. We revealed some factors, which correlated with low activity of catabolic enzymes in ventricular myocardium of the patients with pulmonary embolism: small volume of embolic occlusion (the thromboembolism of lobar and segmental pulmonary arteries); the presence of prior chronic cardiopulmonary disease; the advanced age and the female sex. Preexisting cardiopulmonary disease, as well as age and sex changes of myocardial metabolism, may assist the development of heart failure by relatively small volume of embolic obstruction.

[Structural-metabolic changes in the ventricular myocardium in massive experimental pulmonary embolism]. / Strukturno-metabolicheskie izmeneniia v miokarde zheludochkov pri éksperimental'noi massivnoi legochnoi émbolii.

A comparative study of hemodynamic and structural-metabolic changes in myocardium of right (RV) and left (LV) ventricles by compensative massive pulmonary embolism (MPE) and decompensated MPE was made in 29 mongrel dogs. By decompensated MPE the histoenzymological and ultrastructural methods reveal changes in RV which are not adequate to its high hemodynamic load: the catabolic enzymes activity decreases, the numeral density of mitochondrial profiles decreases too, the fraction of damaged mitochondria increases. By decompensated MPE the myocardial metabolism shifts from catabolic to biosynthetic processes, the activity of NADP.H-D and G-6-PDG increase in both ventricles.

[The functional-morphological state of the myocardium in experimental massive embolism of the pulmonary artery]. / Funktsional'no-morfologicheskoe sostoianie miokarda pri éksperimental'noi massivnoi émbolii legochnoi arterii.

A comparative study of hemodynamic and structural-metabolic changes in the myocardium of the right (RV) and left ventricles (LV) in acute massive pulmonary artery embolism was made in 19 mongrel dogs. In the control group the activity of SDH, MDH, GDH, NADH-DH in LV were higher than in RV. The numeral density and relative area of mitochondrial profile surface in LV was higher that in RV. A significant increase in afterload on RV causes intensification of cell respiration, a rise in numeral density and relative area of mitochondrial profile surface. Weakening of LV work leads to contrary structural-metabolic changes. Thus, contrary changes in hemodynamic loads on RV and LV in acute compensative massive pulmonary artery embolism correlated with contrary changes in their cell metabolism.

[Modeling of massive embolism of the pulmonary artery in experimental animals]. / Modelirovanie massivnoi émbolii legochnoi arterii v éksperimente.

In anesthesized dogs with closed chest and natural respiration massive embolism of pulmonary artery has been simulated with the aid of marked muscular emboli. In 6 h after massive pulmonary embolism pressure in the lesser circulation somewhat decreased, however, it was higher than the initial and control data.

[The systemic and regional changes in the modelling of a massive pulmonary artery embolism]. / Sistemnye i regionarnye izmeneniia pri modelirovanii massivnoi émbolii legochnoi arterii.

In anesthetized dogs with natural breathing, embolisation of pulmonary arterial bed increased systolic pressure in the right ventricle of the heart up to 60.0-113.0 mm Hg. Within 6 hrs the pressure far exceeded initial and control parameters in the minor circulation circle. Tachycardia and tachypnea as well as a reduction of the left ventricle contractions and a decrease of arterial pressure occurred. The massive emboli was followed by an obvious hypoxia and an insignificant hypocapnia with no essential shifts in the blood acid-base balance. Subsequent interstitial oedema of pulmonary tissue may be due both to the changes in the lung hemodynamics and to direct damaging of endothelium in the microvessels.