Objective: to evaluate the relationship of postresuscitation changes in the level of bFGF protein expression and morphological patterns of the cerebellar Purkinje cells.

Materials and methods. Albino adult male rats were subjected to 10 minutes of systemic circulatory arrest caused by cardiac vascular fascicle ligation. The status of a hypoxiasensitive neuronal population of cerebellar Purkinje cells were investigated in different postresuscitation periods. Total numbers of Purkinje cells per mm of their layer length were estimated by a histological analysis of the specimens stained with cresyl violet after the Nissl procedure. An immunocytochemical analysis was performed to determine the number of bFGFpositive (weakly and strongly stained) and GDNFnegative neurons per mm of their layer length and the total population density.

Results. Dynamics of the process of neuronal death and changes of bFGF expression level in the population of the Purkinje cells were determined postresuscitation. Next day after the resuscitation the level of expression of bFGF in the neuronal population significantly increased. At the same time point, the neuronal death did not occur. However, on day 4 the level of bFGF expression decreased and overall density of the population declined. Immunohistochemical study revealed that bFGFnegative cells undergone death. In the later stages of the process postresuscitation (days 7 and 14) the bFGF expression level increased again. At the same time deepening and/or enhancing of the pathological changes in the neuronal population were not observed.

Conclusion. The data indicate that ischemiareperfusion significantly affect the expression of bFGF protein, inducing its elevation within the Purkinje cell population of resuscitated animals. The initial rise in the level of bFGF protein within the neuronal population might prevent the development of a nerve cell death process. The subsequent reduction in the bFGF level is accompanied by the neuronal loss. Therefore, the ability to produce bFGF is an important factor affecting the resistance of neurons to postresuscitation damage. Moreover, the bFGF is considered as promising candidate molecule for developing alternative therapeutic strategies to prevent and/or treatment posthypoxic encephalopathies.

Objective is to identify the pathogenic factors for progression of pancreatogenic cardiac failure in the nearest and remote periods.

Materials and methods. The study was carried out on 130 male Wistar rats (292±4.0 g) divided into 4 groups. The animals were anesthetized with ethyl ether. Acute destructive pancreatitis was simulated in three experimental groups by infusion of bile (0.15 ml/kg body weight) taken from the bile duct into the pancreatic tissue. The isolated isovolumically contracting rat heart (according to E. L. Fallen et al) was simulated 24 hours, 7 days and 1 month after the bile infusion. The pressure in the left ventricle was measured by electric manometer BMT and registered along with the first derivative at the device N3384P calculating the systolic and diastolic blood pressure, and the speed of contraction and relaxation. At the same time the perfusate samples passed through the coronary arteries were har vested, and aspartate aminotransferase (AST) and glucose were determined by standard methods. To identify the cardiac depression, the high contraction rhythm and hypercalcemic and hypoxic perfusion were applied.

Results. It was found that in acute destructive pancreatitis the power and speed parameters of the heart con tractile function were altered that led to lowering the systolic blood pressure and velocity of contraction and relax ation of the left ventricular myocardium and increased diastolic blood pressure as an indicator of cardyomyocyte contracture rate. These abnormalities were evidently manifested in increased heartbits, including hypercalcemic and hypoxic perfusion of the isolated hearts. Glucose consumption was raised per each mmHg generated by the ventricular pressure.

Conclusion. the most significant pathogenetic factors of pancreatogenic heart failure include hypoxia, car diomyocyte membrane destruction, inhibition of sarcolemma Capump, sarcoplasmic reticulum, and mitochondrial dysfunction. The maximum depression of myocardial contractility of the left ventricle is detecting during the first day and in a month after simulated pancreatic necrosis.

Objective: To determine the pathogenic significance of iron ions in the activation of free radical oxidation in trau matic disease and valuate the efficacy of Desferal in the complex therapy of patients with femoral and pelvic fractions.

Materials and methods. Iron metabolism and the intensity of free radical oxidation have been studed in 30 patients with traumas. The patients were randomized into two groups by gender, age and the severity of injury. Group I (n=15) included the injured patients who received the standard intensive therapy. Group II (n=15) included the patients who were treated with Desferal of 8 mg/kg twice daily in 12 hours along with the intensive therapy. The control group comprized of 10 healthy individuals of the same age. The concentration of total and free hemoglobine, serum iron, transferrin, total antioxidant activity of blood serum, the intensity of free radical oxida tion by the Fe2+induced chemiluminescence and hemostatic parameters were studied on admittance as well as on 3rd and 5th day of hospitalization. The parameters of sistemic hemodyamics were checked by integral rheovasog raphy. Statistical processing of data was carried out using Biostat and MS Excel software. The results were pre sented as a mean and standart deviation (M±δ). The Student’s (t) and MannWhitney tests were used to prove the hypotheses. The critical level of significance was P=0.05.

Results. It was determined that the disorders of iron metabolism in patients with traumatic disease were accompanied by intra and extravascular hemolysis, the excess off reduced iron ions catalizing the free radical oxidation, and failure of antioxidant system and disorders of hemostatic system and central hemodynamics. Desferal lowered the level of reduced iron in blood serum, diminished the intensity of free radical oxidation and eliminated the disorders in hemostasis and systemic hemodynamics.

Conclusion. Data confirm the pathogenic role of iron ions in the development of traumatic disease and demon strate the potential of Desferal to correct the traumainduced alterations of oxidantantioxidant system in patients with femoral and pelvic fractions.

The aim of the study was to evaluate the effect of the succinatecontaining antioxidants Reamberin and Cytoflavin on (1) free radical oxidation of lipids and functioning of the antioxidant system in patient with alcoholic liver disease and hepatic encephalopathy and (2) severity of hepatocellular dysfunction.

Material and methods. Prospective study involved 150 patients with alcoholic liver disease divided into three groups: Group 1 (n=50), Group 2 (n=50) and the control group (n=50). Patients of two main experimental groups (Group 1 and Group 2) received antioxidants in addition to conventional basic therapy: patients of Group 1 were administered with Reamberin, whereas in Group 2 Cytoflavin was administered. Intensive care for the patients of the control group did not include any antioxidants. The study involved assessment of the clinical course of hepat ic encephalopathy, biochemical markers of hepatic cell dysfunction, and indicators of lipid oxidation and antioxi dant defense system of the body. Nonparametric statistic methods were used for evaluation of the results.

Results. All examined patients had an increased intensity of free radical oxidation of lipids and low general antioxidant activity demonstrating oxidative distress. Patients from groups 1and 2 exhibited significant improve ment in cognitive and motor functions, positive dynamics of the clinical course of the disease and hepatocellular dysfunction. There was also a trend towards normalization of free radical oxidation of lipids antioxidant para metrs of blood.

Conclusion. Administration of succinatecontaining drugs in alcoholic liver disease resulted in reduction of the period of patients' stay at the Intensive Care Unit and improved longterm effects manifested as prolonged periods of clinical remission of hepatic encephalopathy.

Objective: to demonstrate the course of early period of postnatal adaptation of a premature newborn born from a mother with type 1 diabetes mellitus (T1DM), characterized by abnormal glucose and lipid metabolism. Adverse factors included complications during pregnancy.

Conclusion. Medical examination of the newborn born from a mother T1DM included the assessment of glycemic profile and a full evaluation of metabolism, including lipid metabolism. Respiratory therapy was selected based on clinical and laboratory data. The aim of care was normalize the metabolism and eliminate hypoxia and its consequences as soon as possible. The highfrequency oscillatory ventilation was the possible priority in the selection of mechanical ventilation mode, which allowed to quickly eliminate hypoxia. This strategy resulted in reconstitution of spontaneous breathing, the normalization of metabolism and stabilization of the newborn's condition by the end of the early neonatal period.

The aim was to identify the risk factors contributed to adverse outcome of myocardial infarction (MI) in the acute period of the disease at a prehospital stage.

Materials and methods. The study included the call cards of specialized resuscitation and anesthesia units of the budgetary institution A. S. Puchkov «Station of emergency medical care», to patients with complicated MI. The study included two groups of patients. The first group comprized of patients with complicated MI which resulted in circulatory arrest (n=184), the second group (the group of comparison) included patients with com plicated MI without the outcome in circulatory arrest (n=271). Statistical processing of the material: significance of differences between two binomial observations was evaluated by the Barnard's Exact Test.

The results of the research. The presence of risk of MI complication as a stopping of blood circulation was confirmed in patients of the age group of 40—60 years (P=0.01). Patients with MI complicated by a circulatory arrest was characterized by a significantly greater intensity of pain syndrome (the pain intensity of 9—10 points was typ ical for 11,2% and 3% of patients of the group with circulatory arrest and the group of comparison, respectively; P< 0.001). The combination of clinical manifestations of alveolar pulmonary edema and arrhythmia occurred in 50% of patients with circulatory arrest, resulted in poor prognosis (the frequency of same parameters in a control group was 28,7%, P=0.018). Tachysystolic arrhythmia was the most common form of alteration at a circulatory arrest.

Conclusions. The risk factors for MI adverse outcome in acute period included age from 40 to 60 years, pain of high intensity, presence of cardiogenic shock in combination with alveolar pulmonary edema and tachyarrhythmia.