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.

Adrenal Glands↗

PubMed1993

[The neurohormonal changes in acute pulmonary embolism (clinico-experimental research)].

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.

Acute Disease↗

PubMed1992

[Structural-metabolic changes in the ventricular myocardium in massive experimental pulmonary embolism].

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.

Acute Disease↗

PubMed1992

[Clinico-experimental study of histoenzymological changes in the ventricular myocardium in pulmonary embolism].

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.

Adult↗

PubMed1992

[Lesions of ventricular cardiomyocytes in experimental massive pulmonary embolism].

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.

Animals↗

PubMed1992

[Changes in the dehydrogenase activity of the cardiomyocytes in experimental acute massive pulmonary embolism].

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.

Acute Disease↗

PubMed1991

[The functional-morphological state of the myocardium in experimental massive embolism of the pulmonary artery].

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.

Acute Disease↗

PubMed1990

[The systemic and regional changes in the modelling of a massive pulmonary artery embolism].

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.

Acute Disease↗

PubMed1990

[Modeling of massive embolism of the pulmonary artery in experimental animals].

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.

Animals↗

PubMed1990

[The use of the deep femoral artery for restoring the blood circulation in the leg in the case of a gunshot wound].

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Adult↗

PubMed1990

[Hemodynamic changes in pulmonary thromboembolism].

Three variants of hemodynamic reaction to massive thromboembolism of the pulmonary artery are encountered--hyperkinetic, eukinetic, and hypokinetic. Their manifestations are determined by the patient's cardiovascular status at the onset of thromboembolism, the volume of the embolic obstruction, the degree of pulmonary hypertension, and the concomitant cardiopulmonary pathology. Effective treatment leading to marked reduction of pulmonary hypertension is conducive to increase in the proportion of the hyperkinetic type; ineffective thrombolysis, thrombosis of the inferior vena cava antiembolic filter, recurrent thromboembolism, and infarction pneumonia are the causes of diminished right-ventricular systolic function and reduced cardiac index, i. e. the formation of a hypokinetic type.

Adult↗

PubMed1990

[Hemorheology and blood thrombotic potential in pulmonary thromboembolism].

Examination of 138 patients with acute venous thrombosis of the lower limbs, which was complicated by thromboembolism of the pulmonary artery in 49 of them, showed the rheologic status to be disturbed to a greater extent in patients with pulmonary embolism than in those with acute venous thrombosis. An interrelationship between the rheologic properties and the coagulation system of the blood in various conditions of the hemostasis system was revealed. It is pointed out that pathogenetically grounded correction of the disorders of the blood coagulation and rheologic systems is necessary in choosing the method for treatment and prevention of acute venous thrombosis and pulmonary embolism.

Acute Disease↗

PubMed1988

[Massive thromboembolism of the pulmonary artery].

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Combined Modality Therapy↗

PubMed1988

[The role of local factors regulating vascular blood flow in the development of hypoxia of the gastric mucosa in peptic ulcer].

In 50 patients with gastric ulcer indices of oxygen tension (pO2) levels were investigated in correlation with the concentration of prostaglandins (E and F2 alpha), prostacyclin, thromboxane as well as with values of transmucous difference of potentials in different parts of the gastric mucosa, they were compared with 30 healthy controls. It has been assumed that the detected increase of reverse diffusion of hydrogen ions (the appearance of positive values of the transmembranous potential) and disorder of the ratio of prostanoids in favor of vasoconstrictors lead to a decrease in the blood flow and pO2 in the periulcerative zone of the patients with gastric ulcer. Hypoxia of the gastric mucosa is regarded as an important pathogenetic factor of ulcerogenesis.

Adult↗