The article presents comparative evaluation of serum total oxidizing and total anti-oxidizing activity in reanimation patients with severe cranio-cerebral injury and ischemic and hemorrhagic strokes. Due to irregularity of experimental groups in a number of demographic and clinical indicators the new estimated indicator was proposed. The normalized coefficient of oxidation made it possible to apply comparative evaluation of expression of oxidative anti-oxidative imbalance in these groups. The characteristics are presented concerning the oxidative derangements in the studied groups during acute period of disease.

Objective: to study the time course of changes and an association of contact factors and their inhibitors with the global values of hemocoagulation, fibrinolysis, and inflammatory reactants in acute severe brain injury (SBI) in order to deepen notions of Hageman factor system functioning. Subjects and methods. One hundred and thirteen patients with SBI were examined on 1 to 21 days of injury. The level of unconsciousness averaged a Glasgow coma score of 6.8±0.25. A control group included 23 healthy individuals. The investigators determined the activity of contact factors (prekallikrein, high-molecular-weight kininogen, factors XII, XI) and their inhibitors (total activity of the protein C system, the activity and quantity of antithrombin III, C1 esterase inhibitor, a^antitrypsin, fl^-antiplasmin, fl^-macroglobulin), hemostatic parameters (blood fibrinolytic activity by an euglobulin test; factor XII-kallikrein-dependent fibrinolysis, treptokinase induced fibrinolysis by calculating the plasminogen reserve index, activated partial thromboplastin time, fibrinogen, D-dimer, and soluble fibrin monomer complexes), and inflammatory reactants (C-reactive protein, IL10, IL2, IL4, IL5, IL6, IL8, IL10, IL12p70, TNF-a, and IFN-y). Results. The acute period of SBI was marked by significant deficiency and imbalance of contact factors and their physiological inhibitors. In SBI, prekallikrein rather than factor XII plays a central role in the function of the contact factor system due to inflammatory inhibition of Hageman factor synthesis, which disturbs its key role in the reactions of contact activation of homeostatic proteolytic systems. Out of the considered systems, the activation of which is associated with contact factors, the function of the internal mechanism of fibrinolysis is largely changed; at the same time the internal hemocoagulation activation pathway remains virtually intact. When an inflammatory reaction develops after SBI, normal Hageman factor system protein relationships are impaired. There is the inflammatory inhibition by cytokines, including IL12p70 that is of the greatest importance, which plays a significant role in reducing the level of contact factors and a number of their inhibitors. Key words: severe brain injury, Hageman factor system, antiproteases, inflammation, cytokines.

Objective: to study the oxygen transport system in the acute period of ischemic stroke (IS). Subjects and methods. Central hemodynamics and the oxygen transport system were studied, intracranial pressure was measured, cerebral perfusion pressure was calculated and neurophysiological and X-ray studies were conducted in 36 patients in the first 7 days of IS. Results. In the first 5 study days, circulatory hypoxia developed due to evolving hypodynamic circulation. Later on, the situation was deteriorated by arterial hypoxemia due to acute respiratory distress syndrome and increased pulmonary shunting. Simultaneously on days 5 and 7, there were reductions in the oxygen consumption index and oxygen extraction coefficient, which was due to vasoconstriction, higher blood flow velocity, and lower oxygen extraction. Neurophysiological evidence was used to diagnose sub- and decompensation of stem structural functions. Conclusion. Vasoconstriction leads to the development of circulatory hypoxia. Thus, the early period of ischemic stroke is marked by the decreased oxygen delivery index due to the development of hypodynamic circulation. This is further attended by pulmonary complications and microcircula-tory disorders. On day 5 of the acute period, noncardiogenic pulmonary edema developed and pulmonary shunt increased, by worsening hypoxia. Impaired function of stem structures due to their damage, as evidenced by clinical, neurophysiologi-cal, radiological, and autoptic studies, is one of the causes of hemodynamic disorders, thereby impairing the oxygen transport system. Key words: acute cerebral circulatory disorder, oxygen transport system.

Objective: to study the time course of changes in oxidative status parameters and their relationship with inflammation mediators in the acute period of severe brain injury (SBI). Subjects and methods. One hundred and thirteen patients aged 17—67 years were examined. The injury was closed and open in 54 (47.8%) and 59 (52.2%) patients, respectively. Severe brain contusions were observed in 47 patients, diffuse axonal lesions were seen in 2, and intracranial hematomas were present in 64 patients. The Glasgow coma scores for admission consciousness loss were 6.8±0.25. A control group comprised 23 healthy individuals. The significance of differences was estimated by Student’s test, Wilcoxon-Mann-Whitney, test, Spearman’s correlation test. Venous blood samples were used to study total oxidative activity (TOA) and total antioxidative activity (TAA), diene conjugates, lactic acid, albumin, transferrin (TF), ceruloplasmin, C-reactive protein, and lactoferrin (LF) were measured in venous blood on disease days 1, 4, 7, 10, 14, and 21. The profile of plasma cytokines (IL-1j8, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12p70, TNF-а, and IFN-y) was studied by flow fluorometry on a Cytomics FC 500 cytofluorometer (Beckman Counlter, USA) (reagents were from Bender Medsystems, Austria). Results. In SBI, there was an increase in oxidants, a reduction in antioxidant activity, and lipid peroxidation activation, which were closely related. The oxidation coefficient (TOA/TAA) was 40 times greater than the normal values on days 7 to 10. The oxidation parameters were found to be associated with inflammation and cytokine-mediated immunological reactions. The time course of changes in the study proteins was characteristic for systemic inflammation and there was an association with oxidative processes only for ceruloplasm. TF was found to have an association with IL-5 and IL-10, which reflects its involvement in immunological reactions. The association with hypoxia was established for IL-6 and LF. Ihe elevation or LF was directly caused by the neutrophil activating factor IL-8. Conclusion. Oxidative stress is an important factor in impairing hemostasis in SBI. The processes of oxidation and antioxidation are associated with inflammation and cytokine-mediated immunological reactions. Key words: severe brain injury, oxidative stress, cytokines, acute inflammation phase proteins.

Objective: to study the time course of immunological changes in patients with acute severe brain injury (SBI) and their use along with the integrated indices of evaluation of its severity to define criteria for predicting the development of pyoseptic complications. Subjects and methods. Immunological parameters were studied in 53 SBI patients aged 17—65 years on days 1, 7, and 14 days after injury. There were 2 groups: 1) 16 patients without complications; 2) 37 patients with pyoseptic complications in the acute period of the disease. The integral scales SIRS, CPIS, Glasgow coma scale (GCS), APACHE II, laboratory parameters (immunograms, platelets, soluble fibrin-monomer complexes, and medium molecular weight peptides) in the prediction of pyoseptic complications were analyzed in patients with SBI. A control group consisted of 23 apparently healthy individuals. Results. The found immunological parameters lead to the conclusion that patients with SBI had significant immunodeficiency of mixed genesis by the cellular and humoral types in the acute period of the disease, immune system activation at week 2 of the disease in the development of pyoseptic complications. The decrease in the immunoregulatory index or less than 1.17 or its increase or more than 2.55 on day 1 after SBI was associated with the higher risk of pyoseptic complications. Some indices of an immunogram and the integral scales APACHE II, SIRS, CPIS, and GCS were found to be of low importance in the prediction of pyoseptic complications in SBI. Multivariate regression analysis showed that indices, such as the relative blood count of CD3+, CD95+ lymphocytes, platelets, the serum levels of immunoglobulin M and medium molecular weight peptides (at 262 nm), as well as GCS scores and the maximum temperature on the day of the investigation, were of the greatest value in the construction of prognostic models. Conclusion. The proposed models for the prediction of pyoseptic complications in the acute period of SBI may be useful in optimizing the use of antibiotics and immunomodulating therapy. Key words: severe brain injury, prediction of pyoseptic complications, cellular and humoral immunological parameters.

Fifty-three patients aged 17-65 years who had severe brain injury (SBI) were examined and randomized to 2 groups: 1) 16 patients without complications; 2) 37 patients developed pneumonia (35.2%), bronchitis (32.4%), meningitis (10.8%), meningitis concurrent with pneumonia (8.1%), bedsores concurrent with bronchitis (13.5%) on days 4-7. The authors studied the immune status: the subpopulation composition of lymphocytes (CD+, a marker of adult lymphocytes; CD+, a marker of T helper/inductor cells, CD8+, a marker of cytotoxic lymphocytes, CD16+, a marker of natural killer cells, CD20+, a marker of B lymphocytes) by the indirect immunofluorescence technique using monoclonal antibodies; the functional activity of lymphocytes from the expression of activation antigens, such as CD71+, CD25+, HLA-DR; serum immunoglobulins (IgG, IgA, and IgM) by the immunoturbidimetric technique using the test systems (Spinreakt, Spain). A control group included 23 apparently healthy individuals. Immunosuppression developing as significant T lymphopenia due to lower CD4+ and CD8+ lymphocytes, as well as impaired humoral immunity with inadequate IgG generation was detected in the acute phase of SBI. The indicators reflecting the development of secondary pyoseptic complications were elevated CD3+, CD4+, and CD8+ lymphocytes on day 7 and the higher lymphocytic expression of the activation antigens CD25+ and CD71+. The findings show that the diagnostic markers, such as CD3+, CD4+, CD8+, CD25+, and CD71+ lymphocytes, should be included into a comprehensive examination of patients with SBI.

Objective: to study the time course of changes and relationship of the serum indicators of apoptotic processes in neurore-suscitation patients. Subjects and methods. Thirty-eight neuroresuscitation patients, including 14 patients with severe brain injury (SBI) (mean age 41.4±4.3 years) and 24 patients with strokes (mean age 53.8±2.5 years), were examined. The group of patients with strokes was divided into 2 subroups: 1) 11 patients with ischemic strokes (IS) and 2) 13 with hemorrhagic strokes (HS). The Glasgow coma scores for admission consciousness loss were 7.6±0.8 in the SBI group and 9.5±0.7 in the stroke group; mortality was 28.6 and 37.5%, respectively. A control group included 16 subjects (mean age 47.9±3.8 years). The investigators measured the serum levels of FAS antigen and its ligand (sAPO-I/FAS and sFAS-L), cas-pase-1/ICE, sCD40 (Bender MedSystem, Austria) and hTRAIL (Biosource, Belgium) by solid-phase immunoassay in neuroresuscitation patients on days 1, 7, and 14 of the acute period of diseases. They used statistical methods, such as Wilcoxon-Mann-Whitney U-test, Spearman’s rank correlation test. Results. A reduction in hTRAIL was observed in all the groups. There was a decrease in serum sCD40 in strokes on days 1 to 14 and in SBI on days 7 to 14. An increase in caspase 1/ICE was seen in HS in the first 24 hours, in IS on days 1 to 7, and in SBI on days 1 to 14. The most pronounced rise in caspase-1/ICE was induced by ischemic brain lesion within the first week of disease. A prolonged increase up to 2 weeks was noted in SBI. No rise in serum FAS-L was found in the examinees. The time course of changes in sAPO-I/FAS was different in all the groups. The most marked, moderate, and none reductions were revealed in HS, IS, and SBI, respectively. There was a pronounced serum sAPO-I/FAS increase in SBI within the first 24 hours. Assessment of correlations between the serum indicators of apoptosis revealed that there were differences in the association between the indices under study in all the patient groups and in the control group. Conclusion. There are general features and differences in the time course of changes in serum apoptotic markers and their association in the acute period of SBI, IS, and HS. Key words: severe brain injury, stroke, apoptosis, APO-I/FAS, FAS-L, caspase-1/ICE, CD40, hTRAIL.

Objective: to study the central hemodynamics (CH) and intracranial and cerebral perfusion pressures (ICP and CPP) in acute cerebral circulatory disorders (ACCD) and their possible relationships for further development of intensive differential therapy for the detected disorders. Material and methods. Hemodynamic studies using the transpulmonary thermodilu-tion technique, measurements of ICP, calculations of CPP, and currently available X-ray studies were conducted in 18 patients on days 1, 3, 5, and 7 of ACCD. All the patients were found to have essential hypertension and coronary heart disease. Results. In the first 5 days of ACCD, there was a normodynamic type of circulation in hemorrhagic stroke (HS) and a hypodynamic type in ischemic stroke (IS). ICP remained at the baseline elevated level in the IS group and increased over time in the HS group. CPP was significantly unchanged. Myocardial dysfunction was detected when there was a significant preload caused by a high postload. In IS, an inverse correlation was found between ICP and global ejection fraction (GEF), cardiac performance index (CPI) and on day 7, the correlation was direct. In HS, ICP had a direct correlation with CPI and an inverse correlation with GEF. These changes during treatment failed to progress and were revealed in the presence of brain dislocation, as evidenced by spiral computed tomography. Conclusion. Thus, the pattern of CH disorders depends on the type of ACCD. In the first 5 days of ACCD, a hypokinetic circulatory type is registered in IS and a normokinetic type is in HS. Evolving dislocation of the brain with impaired function of its stem structures due to ICP elevation is one of the causes of central hemodynamic changes. The value of ICP in ACCD is a crucial indicator in the diagnosis of secondary brain damages and determines treatment policy. Key words: acute ischemic attack, intracranial pressure, cerebral perfusion pressure, central hemodynamics, myocardial depression.

Objective: to evaluate changes in the laboratory markers of endogenous intoxication in acute severe brain injury (SBI) and to define their prognostic significance in the development of pneumonias. Subjects and methods. Sixty-six patients with isolated severe brain injury in the acute phase of the disease were examined and divided into two groups: 1) 35 (53%) patients who were not observed to have pneumonias in the acute period; 2) 31 (47%) who had developed pneumonia on an average of 7.7±2.8 days after injury. Endogenous intoxication was evaluated from the erythrocytic sedimentation rate (ESR), leukocytic indoxication index (LII), the spectrum of serum medium molecular-weight peptides and red blood cells, complements C3, C4, C-reactive protein, soluble fibrin monomer complexes, dienic conjugates, lactic acid, urea, and creatinine. Immunological parameters, such as the total count of lymphocytes and the level of CD3+ lymphocytes (a marker of mature lymphocytes), were studied by indirect monoclonal antibody immunofluorescence. A control group comprised 24 healthy individuals. The data were statistically processed by the Statistica-6 program, by applying Student’s test, and Pearson’s correlation coefficient. Results. Endogenous intoxication was found to be attended by immunodeficiency and to show two waves; just after injury it was caused by diseased and ischemic brain tissue destruction products and its second wave was associated with the development of pneumonias by the end of the first week after injury when an increase in proteolysis products along bacterial toxemia proved to be of significance. The markers, the predictors of pneumonia development in SBI, are increases in ESR up to more than 40 mm/hour on day 3, ESR up to more than 50 mm/hour, and in complement C3 levels up to more than 1.5 g/l on day 5. The early markers of pulmonary complications are increases in serum medium molecular-weight peptide levels up to over 0.3 optical density units at 262 nm, in C-reactive protein up to more than 100 mg/l, and in dienic conjugates up to above 1.2 mmol/l on day 7. The good predictor of the course of pneumonia is an increase in complement C4 levels up to over 0.4 g/l after day 7 and a reduction in LII to less than 3 relative units. Conclusion. The findings show it necessary to include the diagnostic markers: medium molecular-weight peptides, C-reactive protein, and dienic conjugates into the comprehensive examination of patients with severe brain injury. Key words: severe brain injury, endogenous intoxication, C-reactive protein, dienic conjugates, medium molecular-weight peptides, pneumonias.