[Changes in generation of superoxide anion-radical by phagocytic and other cells of atherosclerotic plaques at different stages of human atherosclerosis]. / Dinamika generatsii superoksidnogo anion-radikala fagotsitiruiushchimi i drugimi kletkami ateroskleroticheskikh bliashek na raznykh stadiiakh aterogeneza u cheloveka.

We investigated changes in generation of free radicals of oxygen including superoxide anion-radical (SAR) of oxygen by phagocytes and other cells of atherosclerotic plaques resected in operations of aortofemoral or aortoiliac bypass grafting and plastic vascular surgery of 38 patients with obliterating atherosclerosis obliterans of the lower extremities. We found some regularities in changes of SAR generation by phagocyting cells of atherosclerotic plaques at different morphological stages of their formation. Generation of the radicals progressively increased at the stage of fibrous plaques (1.56 times vs control), increased still more at the stage of their atheromatous alterations (2.3 times) and noticeably decreased at the stage of their calcinosis. Simultaneously, there was intensification of SAR formation by non-phagocyting cells of atherosclerotic plaques under their stimulation by NADPH-H (in fibrous and atheromatous plaques 1.3 and 2.0 times, respectively). On the contrary, at calcinosis stage NADPH-stimulated radical generation by these cells reduced.

[Clinical significance of interaction between Chlamydia infection (Chlamydia pneumoniae) and free radical processes during ischemic heart disease]. / Klinicheskoe znachenie vzaimodeistviia khlamidiinoi infektsii (Chlamydia pneumoniae) i svobodno-radikal'nykh protsessov pri ishemicheskoi bolezni serdtsa.

AIM: To determine occurrence and activity of chlamydial infection (CI) as well as activity of free radical processes in clinical course of different forms of ischemic heart disease. MATERIAL AND METHODS: 34 coronary heart disease (CHD) patients entered the study. 23(67.6%) of them had effort angina and unstable angina, 11(32.4%) patients had non-Q myocardial infarction (19 men and 15 women). 14 healthy donors served control. CI was detected with enzyme immunoassay. The examinations were made in exacerbation and 2 weeks later in clinical improvement. Chlamydia pneumoniae infection in the tissues of the aorta and left coronary artery was studied in 15 dead bodies using the polymeric chain reaction. Generation of active oxygen forms by leukocytes was tested by luminol-dependent chemiluminescence method. In addition, the patients and donors were examined for malonic dialdehyde. RESULTS: Titers of IgA and IgG of C. pneumoniae antibodies were high in CHD exacerbation. IgM antibodies were not found in the diagnostic titers. Follow-up values of IgA and IgG titers lowered. C. pneumoniae was found in 12 of 15 autopsy specimens. Basal and stimulated indices of leukocytic generation of active oxygen forms in patients with CHD exacerbation were higher than in donors. Later, the generation declined. Malonic dialdehyde was also elevated in the exacerbation and lowered in clinical improvement. A correlation exists between IgA and IgG antibodies titers and chemiluminescence intensity in CHD exacerbation. CONCLUSION: In progression of atherosclerotic process including CHD and its exacerbations CI and free radical processes activate. These may be related showing a feasibility of C. pneumoniae involvement in development of atherosclerosis.

[The antioxidant protection of the heart by coenzyme Q10 in stable stenocardia of effort]. / Antioksidantnaia zashchita serdtsa koénzimom Q10 pri stabil'noi stenokardii napriazheniia.

It was found that patients with angina of effort (functional class II and III) exhibit enhanced generation of active oxygen forms by leukocytes, higher concentration of malonic dialdehyde in plasma and lower antiperoxide resistance of plasma. These changes increase with increasing severity of the disease. Adjuvant use of coenzyme Q10 in combined antianginal therapy suppresses generation of active oxygen forms by leukocytes, lipid peroxidation. Antiperoxide plasma resistance rises. In this way clinical improvement of effort angina is achieved.

[The role of the lungs in regulating the generation of active forms of oxygen by the phagocytes, the concentration of immunoglobulins and the complement activity]. / Rol' legkikh v reguliatsii generatsii aktivnykh form kisloroda fagotsitami, soderzhaniia immunoglobulinov i aktivnosti komplementa.

Experiments on 25 intact dogs, 2 calves and clinical tests in 45 patients have shown that in the blood of the aorta or pulmonary vein leaving the lungs there is a rise in generation of active oxygen forms by leukocytes, their phagocytic activity, the activity of myeloperoxidase, NADPN-oxidase, complement, immunoglobulins content. As to the liver, kidneys, spleen, no such increased generation of active oxygen forms by leukocytes was registered. The results suggest an important role of the lungs in regulation of free radical activity of leukocytes, their phagocytic ability and thus in anti-infection defense of the body.

[Carbon dioxide--a universal inhibitor of the generation of active oxygen forms by cells (deciphering one enigma of evolution)]. / Uglekislyi gaz--universal'nyi ingibitor generatsii aktivnykh form kisloroda kletkami (k rasshifrovke odnoi zagadki évoliutsii).

Studies were carried out on blood phagocytes and alveolar macrophages of 96 humans, on the cells of the viscera and tissue phagocytes (liver, brain, myocardium, lungs, kidneys, stomach, and skeletal muscle), and liver mitochondria of 186 random bred white mice. Generation of the active oxygen forms was determined using different methods after direct effect of CO2 on the cells and biopsies and indirect effect of CO2 on the integral organism. The results obtained suggest that CO2 at a tension close to that observed in the blood (37.0 mm Hg) and high tensions (60 or 146 mm Hg) is a potent inhibitor of generation of the active oxygen forms by the cells and mitochondria of the human and tissues. The mechanism of CO2 effect appears to be realized, partially, through inhibition of the NADPH-oxidase activity. The results are important for deciphering of a paradox of evolution, life preservation upon appearance of oxygen in the atmosphere and succession of anaerobiosis by aerobiosis, and elucidation of some other problems of biology and medicine, as well as analysis of the global bioecological problem, such as ever increasing CO2 content in the atmosphere.

[Ability of carbon dioxide to inhibit generation of superoxide anion radical in cells and its biomedical role]. / Svoistvo uglekislogo gaza ingibirovat' generatsiiu superoksidnogo anion-radikala kletkami i ego biomeditsinskoe znachenie.

The study was carried out on blood phagocytes and alveolar macrophages of 96 persons, cells of inner organs and tissue phagocytes (liver, brain, myocardium, lungs, kidneys, stomach, skeletal muscles), as well as on mitochondria of the liver of 186 non-linear white mice. Generation of active oxygen forms (AOF) was evaluated by various methods with CO2 directly affecting the cells and bioptates and indirectly the whole organism. The results show that CO2 with tension close to that of the blood (37.0 mm Hg) and at higher tensions (60 and 146 mm Hg) is a powerful inhibitor of AOF generation by human and animal cells, as well as by liver mitochondria of mice. The data obtained allow to explain, in terms of AOF role, a number of physiological and pathophysiological (medical) CO2 effects.

[Comparative study of the effect of carbon dioxide on the generation of active forms of oxygen by leukocytes in health and in bronchial asthma]. / Sravnitel'noe issledovanie vliianiia dioksida ugleroda na generatsiiu aktivnykh form kisloroda leikotsitami v norme i pri bronkhial'noi astme.

The study was conducted by using leukocytes isolated from 74 apparently healthy donors and 60 patients with bronchial asthma. The generation of active oxygen forms was determined by luminolo- and lucigenin-dependent chemiluminescence techniques and NTC-reaction. The findings suggest that at the tension close to the blood tension of 37.5 mm Hg and the high tension of 146 mm Hg is a powerful natural inhibitor of leukocytic generation of active oxygen forms. At an exacerbation, the inhibitory effect of carbon dioxide on the leukocytic generation of active oxygen forms decreased in most (70%) patients with bronchial asthma, which potentiates the free radical mechanism of development of bronchial asthma. It may be held that the literature-described use of carbon dioxide for the treatment of bronchial asthma is justifiable only in a lower proportion of patients who have preserved a high sensitivity to the inhibitory effect of carbon dioxide on the generation of active oxygen forms.

[Changes in the sensitivity of leukocytes to the inhibiting effect of CO2 on their generation of active forms of oxygen in bronchial asthma patients]. / Izmenenie chuvstvitel'nosti leikotsitov k ingibiruiushchemu vliianiiu CO2 na generatsiiu imi aktivnykh form kisloroda u bol'nykh bronkhial'noi astmoi.

30 bronchial asthma (BA) patients and 15 donors were exposed to 8.3% and 20.8% CO2 to bring out leukocytes sensitivity to CO2 by generation of active oxygen (AO) in bronchial asthma. CO2 effects on leukocyte AO generation were defined by luminol-dependent chemiluminescence (CL) before and after the exposure to CO2. It was found that in healthy subjects 8.3% and 20.8% CO2 noticeably inhibits leukocyte CL. However, in 70% of asthmatics with BA exacerbation leukocyte sensitivity to CO2 inhibition diminished. This was normal in 30% of BA patients. With BA aggravation, leukocyte sensitivity to CO2 tended to a decrease. Remission brought a complete or partial recovery of the above sensitivity. Thus, on the one hand, CO2 is involved in BA pathogenesis in terms of its inhibitory effect on AO generation by leukocytes; on the other hand, only in 30% of BA patients high CO2 concentrations as a treatment may be justified.

[Intercellular interactions in morphogenesis of initial lesions and sclerosis in interstitial lung diseases]. / Mezhkletochnye vzaimodeistviia v morfogeneze initsial'nykh povrezhdenii i skleroza pri interstitsial'nykh bolezniakh legkikh.

A total of 117 patients with pulmonary interstitial diseases (PID) were examined. The functional activity of alveolar macrophages was assayed in the lavage fluid and in lung tissue biopsy specimens from the generation of active oxygen forms, the secretion of tumor necrosis factor, fibronectin, expression of c-fos- and c-sis-oncoprotein. The stereotypic value for various PID was the development of alveolitis running in 2 stages: 1) early one, including exudative inflammation and 2) late one, involving sclerotic changes up to the formation of the honeycomb lung. This results in the block of the blood-air barrier and progression of respiratory failure and hypoxia in patients. The morphogenesis of fibrosing alveolitis is formed of alveolar septal damages caused by etiological agents of various nature, which is frequently unclear, by active forms of oxygen, lipid peroxidation products, proteases, tumor necrosis factor, which are produced by activated alveolar macrophages and polymorphonuclear leukocytes. The alveolar macrophage that secretes growth factors, c-fos- and c-sis-oncoproteins plays the key role in the progression of sclerotic changes. Lung cancer may develop at the end of fibrosing alveolitis at the stage of the honeycomb lung.

[Variants and stages in the course of idiopathic fibrosing alveolitis]. / Varianty i stadii techeniia idiopaticheskogo fibroziruiushchego al'veolita.

Clinicomorphological analysis covered 41 cases of idiopathic fibrosing alveolitis (IFA). The comparison of the degree of respiratory insufficiency, hypoxia, survival of the patients with cytogram of the bronchoalveolar lavage, morphological findings, generation of active oxygen forms by alveolar macrophages and leukocytes has provided evidence on an important role of alveolar macrophage in interstitial alveolitis and fibrosis in IFA. Three variants of chronic IFA are distinguished: aggressive, persistent and slowly progressive. The variants have different prognosis and need individual therapeutic approach.

[Aevit and glutamic acid in the treatment of patients with bronchial asthma]. / Aevit i glutaminovaia kislota v lechenii bol'nykh bronkhial'noi astmoi.

To elucidate the effect of antioxidants aevit and glutaminic acid on the course of bronchial asthma (BA) and free radical processes in this disease, 54 BA patients were divided into 2 groups: glucocorticoid-untreated and glucocorticoid-treated. Each of two subgroups made of these groups either received antioxidants (AO) or not. The response was assessed by clinical BA symptoms and free radical processes reflecting production of active oxygen forms by leukocytes (PAOFL) and free radical peroxidation (FRPO). PAOFL was studied using luminol-dependent chemiluminescence (CL). CL basal and stimulated values were calculated. FRPO was measured by plasma levels of malonic dialdehyde. Aevit and glutaminic acid treated BA patients improved clinically and exhibited reduced CL of PAOFL and malonic dialdehyde in plasma compared to BA patients on conventional therapy or conventional therapy plus glucocorticoids. Aevit and glutaminic acid are recommended for BA patients.

[The mechanisms of the intensification of free radical processes in patients with IHD-stenocardia in relation to its severity]. / O mekhanizmakh usileniia svobodnoradikal'nykh protsessov u bol'nykh IBS--stenokardiei v zavisimosti ot ee tiazhesti.

The ability of leukocytes to generate active oxygen forms and plasmic levels of malonic dialdehyde as indicators of free radical process activity and that of lipid peroxidation (POL), respectively, were investigated in 50 patients with angina pectoris (20 patients with functional class I-II and 30 patients with functional class III-IV) versus 18 donors. The anginal patients are shown to have enhanced POL and free radical processes which appeared correlated with the disease severity. The authors identify factors intensifying free radical processes in anginal patients: platelet inhibition of leukocytic ability to generate active oxygen forms, changes in plasmic levels of IgM, C-reactive protein, serum iron.