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Presented in the article are the results of studying antiaggregate activity of acetylsalicylic acid and clopidogrel in a total of 36 patients suffering from various-severity chronic arterial insufficiency of lower limbs on the background of atherosclerosis obliterans. The study was conducted prior to treatment for correct selection of a particular antiplatelet agent. The obtained results showed that clopidogrel was not always more efficient than acetylsalicylic acid, since there is individual sensitivity of each patients to a particular antiplatelet agent. Therefore, an individual approach is necessary to conservative therapy of arterial insufficiency of lower limbs. For some patients it is preferable to administer clopidogrel, for others - acetylsalicylic acid. In a series of cases combined treatment is justified, while some patients having low sensitivity to both acetylsalicylic acid and clopidogrel require careful selection of alternative agents influencing other thrombocyte receptors.

The study comprised a total of 107 patients (all men) after endured femoropopliteal bypass grafting above the genicular fissure with a synthetic stent graft manufactured by the Gore Company for stage IIB and III chronic arterial insufficiency of the lower extremities according to the Fontain-Pokrovsky classification. Group One I (control group) was composed of fifty-four patients permanently taking in the postoperative period at the out-patient stage pentoxiphylline (trental 400 mg 1 tablet 3 times daily) and xantinol nicotinate at a dose of 150 mg one tablet thrice daily. Group Two (Study Group) consisted of fifty-three patients taking after reconstructive vascular surgery at the out-patient stage in addition to pentoxiphylline and xantinol nicotinate acetylsalicylic acid (cardiomagnil 75 mg 1 tablet once daily). The Control Group patients within 3 to 6 months of follow up were found to have a considerable progressing improvement of the functional abilities of the microcirculatory bed requiring in 44 (81.5%) cases hospitalization to the Surgical Department for intensive vascular therapy. Despite this fact four (7.4%) patients within the time frame from 6 to 9 months after surgery developed thrombosis of the vascular implant requiring a repeat surgical intervention. In the Study Group patients, the degree of functional capabilities of the microcirculatory bed in the postoperative period was less considerable, reaching the maximum after 10-12 months of follow up, with eighteen (34.0%) patients requiring hospitalization for additional vascular therapy to perform. There were no cases of implants' thrombosis in the Study Group patients. Pathological alterations in the functional state of the peripheral vascular bed correlated with viscosimetric indices and activity of blood platelet aggregation. The addition of antithrombocytic agents to conservative postoperative therapy considerably improved the outcomes of surgical treatment.

Several cases of successful surgical treatment of giant spinal neuromas are reported in this paper. Benign nature of these tumors promotes radical resection. Localization of giant extravertebral tumor nodes in eloquent areas produces difficulties for total removal. In certain cases single approach is not sufficient for radical resection.

Chair of Neurology of the Advanced Medical Training Department of the Federal Educational Facility of the Higher Vocational Education Russian State Medical University under the Russian Public Health Ministry, Moscow, Russia. The article deals with the findings obtained in examining and treating a total of eighty-seven patients suffering from atherosclerosis obliterans of the lower-limb arteries with stage IIB and III chronic arterial insufficiency. Studied were impairments of the theological properties of the blood and plasma, erythrocytic deformability and the concentration of malonic dialdehyde in blood at admission to the hospital, upon completion of the course of conservative treatment, and after the reconstructive vascular intervention performed. It was determined that the leading mechanism disturbing oxygen utilization by tissues is a decrease in erythrocytic deformability, which promotes shunting of the arterial blood flow and persists after the surgical vascular reconstruction preformed.

The work was based on the findings of the examination and surgical management of 69 patients with obliterating atherosclerosis of the lower limbs with various degree of chronic arterial insufficiency. The authors analyzed the main causes promoting development of early reocclusion of the bypasses and prostheses following reconstructive surgical operations. They also proved the role of high peripheral vascular resistance and, in particular, diminished functional possibilities of the microcirculatory-bed vessels in the genesis of early reocclusions in patients with chronic arterial insufficiency of the lower limbs. They also suggested a new technique of determining the carrying capacity of the microcirculatory channel, the use of which in the preoperative period makes it possible to predict development of early thrombotic complications, and in some cases to wisely abstain from carrying out a reconstructive vascular intervention due to high risk of its poor outcomes. It is preferable for such patients to undergo conservative pathogenetic preoperative therapy aimed at improving the functional possibilities of the microcirculatory vessels.

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 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.

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.

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.

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.

State of oxygen consumption in gastric mucosal membrane evaluated by means of pO2 measurement as well as metabolism of cyclic nucleotides were studied in patients with ulcerous disease. Hypoxia of periulcerous area and alterations in functional activity of the cyclase systems were detected. Reciprocal alterations in the cyclases activity, as a result of which the ratio of cyclic nucleotides was changed under dissimilar conditions of oxygen consumption in gastric mucosal membrane, were considered as essential adaptive reaction related to maintenance of proliferation under conditions of oxygen and energy rich substances deficiency.

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.

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.

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.

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.

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.

The investigation of average time of transport of radionuclide along the venous system of lower extremities was used by the authors to assess the evacuation function of the musculo-venous "pump" of the leg in 10 healthy people and 50 patients with varicose disease of lower extremities. The direct relation between the degree of incompetence of the musculo-venous "pump" and the degree of the varicose disease speaks of its obvious pathogenetical role in the development of venous pathology.

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.