[Differential surgical treatment of victims with damage to the small and large intestines in a closed abdominal injury combined, depending on the prediction of traumatic disease course and morphological changes of the intestinal wall].

Use of differentiated surgical approach to the management of surgical treatment, depending on the degree of violation of systemic hemodynamics, the timing and volume of surgical procedures, depending on the prognosis of traumatic disease course of cardiac index, interventions in the small and large intestine depending on morphological changes of the intestinal wall by cardiac and stroke indexes, put method extra-enteric anastomosis in patients with damage to the small intestine and colon combined with closed abdominal injury permitted to reduce the rate of postoperative complications from 22.2 to 10.1%, mortality at 2.1 times in shock period (from 19.3 to 9.2%) and the overall mortality from 33.3 to 21.1%.

Prevention of neurodegenerative damage to the brain in rats in experimental Alzheimer's disease by adaptation to hypoxia.

We report here studies addressing the possibility of preventing neurodegenerative changes in the brain using adaptation to periodic hypoxia in rats with experimental Alzheimer's disease induced by administration of the neurotoxic peptide fragment of beta-amyloid (Ab) into the basal magnocellular nucleus. Adaptation to periodic hypoxia was performed in a barochamber (4000 m, 4 h per day, 14 days). The following results were obtained 15 days after administration of Ab. 1. Adaptation to periodic hypoxia significantly blocked Ab-induced memory degradation in rats, as assessed by testing a conditioned passive avoidance reflex. 2. Adaptation to periodic hypoxia significantly restricted increases in oxidative stress, measured spectrophotometrically in the hippocampus in terms of the content of thiobarbituric acid-reactive secondary lipid peroxidation products. 3. Adaptation to periodic hypoxia completely prevented the overproduction of NO in the brains of rats with experimental Alzheimer's disease, as measured in terms of increases in tissue levels of stable NO metabolites, i.e., nitrites and nitrates. 4. The cerebral cortex of rats given Ab injections after adaptation to periodic hypoxia did not contain neurons with pathomorphological changes or dead neurons (Nissl staining), which were typical in animals with experimental Alzheimer's disease. Thus, adaptation to periodic hypoxia effectively prevented oxidative and nitrosative stress, protecting against neurodegenerative changes and protecting cognitive functions in experimental Alzheimer's disease.

[Prevention of the brain neurodegeneration in rats with experimental Alzheimer's disease by adaptation to hypoxia].

The study focused on a possibility of preventing brain neurodegeneration by adaptation to intermittent hypoxia (AH) in rats with experimental Alzheimer's disease (AD) modeled by injection of a neurotoxic bert-amyloid peptide fragment (Ab) into n. basalis magnocellularis. AH was produ- ced in an altitude chamber (4.000 m; 4 hours daily; 14 days). The following results were obtained after fifteen days of the Ab injection: (1) AH substantially prevented the memory impairment induced by Ab, which was determined using the conditioned avoidance reflex test; (2) the AH significantly restricted the enhanced oxidative stress, which was determined spectrophotometrically by thiobarbituric acid-reactive substance level in the hippocampus; (3) the AH completely prevented Ab-induced nitric oxide (NO) overproduction in brain, which was measured by tissue level of nitrite and nitrate; (4) pathologically changed and dead neurons (Niessle staining) were absent in the brain cortex of rats exposed to AH before the Ab injection. Therefore AH seems to effectively prevent oxidative and nitrosative stress thereby providing protection of brain against neurodegeneration and preservation of cognitive function in experimental AD.

Role of nitric oxide in prevention of cognitive disorders in neurodegenerative brain injuries in rats.

NO synthesis disturbances play an important role in the development of neurodegenerative damage in Alzheimer disease. We previously showed that adaptation to intermittent hypobaric hypoxia prevents cognitive disturbances in rats with experimental Alzheimer disease. Here we evaluated the role of NO in cognitive disorders and development of adaptive protection during experimental Alzheimer disease. Adaptation to hypoxia in rats was performed in a hypobaric pressure chamber at a simulated altitude of 4000 m (4 h per day for 14 days). Alzheimer disease was simulated by bilateral injections of a toxic fragment of beta-amyloid (25-35) into n. basalis magnocellularis. For evaluation of the role of NO in the development and prevention of memory disorders, the rats received intraperitoneally either NO-synthase inhibitor N omega-nitro-L-arginin (L-NNA, 20 mg/kg, every other day for 14 days) or NO-donor dinitrosyl iron complex (200 microg/kg daily for 14 days). NO-synthase inhibitor potentiated the damaging effect of beta-amyloid, abolished the protective effect of adaptation to hypoxia, and produced memory disorders in rats similar to those observed during experimental Alzheimer disease. In contrast, the increase in NO level in the body provided by injections of the NO-donor produced a protective effect against memory disorders caused by beta-amyloid similar to that induced by adaptation to hypoxia. We concluded that reduced NO production in the organism plays an important role in the development of cognitive disorders produced by injections of beta-amyloid, while prevention of NO deficit by administration of NO-donors or non-pharmacological stimulation of NO synthesis can provide a protective effect in experimental Alzheimer disease.

[The effects of adaptation to hypoxia on the resistance to neurodegenerative disorders in the brain of rats of different genetic strains].

The aim of the study was to compare the protective effects of adaptation to altitude hypoxia (AH) on neurodegenerative brain disorders (NBD) induced with infusion of beta-amyloid peptides (Abeta) into the brain (imitation of Alzheimer's disease) of rats belonging to two species: Wistar rats (WR) and August rats (AR). Previously it was shown by the authors that WR were less resistant to memory function impairment and open-field activities, induced with Abeta infusion compared with AR. This study showed that preliminary AH significantly restricted brain function impairment induced by Abeta in WR, so AH demonstrated the protective effect in WR. In contrast, in AR preliminary AH provoked those impairments induced by Abeta. The AH protective effect in WR was associated with activation of stress-limiting systems (antioxidant system, NO system). Lack of AH protective effect in AR was associated with lack of activation of these systems in these rats. Thus, the different AH effects on NBD development in WR and AR are obviously determined by hereditary peculiarities of stress-limiting systems in WR and AR.

Role of heat shock proteins HSP70 and HSP32 in the protective effect of adaptation of cultured HT22 hippocampal cells to oxidative stress.

Preadaptation of cultured HT22 mouse hippocampal neurons to oxidative stress prevented cell damage induced by severe oxidative stress. This protection manifested in a decrease in metabolic disturbances in neurons. Adaptation of neurons to oxidative stress was accompanied by accumulation of HSP32 and HSP70. HSP synthesis inhibitor quercetin abolished the protective effect of adaptation under conditions of oxidative stress. Activation of HSP70 synthesis in neurons is an important mechanism for adaptive protection of cells.

Inversion of stress response reprogramming phenomenon in lipopolysaccharide-stimulated alveolar macrophages.

The stress response and NO production in reprogrammed proinflammatory or antiinflammatory alveolar macrophages were studied after lipopolysaccharide treatment. Experiments with macrophages not containing HSP70 showed that lipopolysaccharide in a dose of 500 ng/ml induced stress response in cells with the proinflammatory phenotype (as distinct from an antiinflammatory phenotype). The stress response was not observed in HSP70-containing lipopolysaccharide-stimulated proinflammatory macrophages, but occurred in cells with antiinflammatory phenotype. Hence, the presence of HSP70 in alveolar macrophages results in the inversion of the phenomenon of reprogramming of the stress response. Independently on the phenotype, stimulation with lipopolysaccharide was accompanied by a 60-70% increase in NO production by macrophages not containing HSP70. However, NO production by HSP70-containing macrophages did not increase in response to lipopolysaccharide treatment. Our results indicate that reprogramming of the cell response in macrophages does not concern the system for NO synthesis. HSP70 prevents the lipopolysaccharide-induced activation of NO synthesis in alveolar macrophages.

Role of extracellular and intracellular nitric oxide in the regulation of macrophage responses.

We studied the role of nitric oxide in the stress response and apoptosis. Intracellular nitric oxide potentiated the stress response. However, intracellular nitric oxide suppressed the stress response in macrophages of proinflammatory and antiinflammatory phenotypes. Intracellular nitric oxide promoted apoptosis in macrophages of the proinflammatory phenotype, but inhibited this process in cells of the antiinflammatory phenotype. Exogenous nitric oxide synthesized by macrophages protected them from lipopolysaccharide-induced apoptosis. Our results indicate that nitric oxide produces various effects on the stress response and apoptosis in macrophages, which depends on modus operandi.

Resistance to neurodegenerative brain damage in August and Wistar rats.

In Wistar and August rats characterized by different resistance to acute emotional stress we compared the resistance to neurodegenerative brain damage (model of Alzheimers disease) produced by administration of a neurotoxic peptide fragment (25-35) beta-amyloid into the brain. August rats were more resistant to acute stress and development of neurodegenerative disorders compared to Wistar rats. This conclusion was derived from studying animal behavior in conditioned passive avoidance task and open-field test that characterize cognitive function of the brain. Administration of beta-amyloid modulated the behavior of Wistar rats, which reflected the impairment of memory and orientation and exploratory activity in these animals. These disturbances in Wistar rats were accompanied by activation of lipid peroxidation in the hippocampus.

[The extent of resection in rectal cancer]. / Ob urovne rezektsii pri rake priamoi kishki.

The condition of the "tumor field" in cancer of the rectum was studied. The work was performed on 28 preparations of the resected and extirpated rectum as serial paraffin sections in 8 radial directions for a distance of 10 cm from the visible margin of the tumor. The "tumor field" border at the distal direction is not less than 3.5-4 cm with the exophital growth and 4-5 cm with the endophital growth. The "tumor field" contours resemble an ellipse with excentricity in the proximal direction.

[Comparative evaluation of proximal resections in rectal cancer]. / Sravnite'lnaia otsenka proksima'lnykh rezektsii po povodu raka priamoi kishki.

The surgical treatment of rectum cancer in 165 patients with the apparatus AKA-2 for compressive anastomoses was analyzed. The oncological adequacy of proximal resections of the rectum at the distal level of the section not less than 3.5-5 cm from the visually seen margin of the tumor depending on its growth type was shown. Low anterior resection of the rectum in patients with considerable size of the tumors is not oncologically justified.