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.

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 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 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.