蕲蛇酶配以高压氧治疗急性脑梗死疗效分析

目的 探讨治疗急性脑梗死有效的方案。方法 观察发病在４８ｈ内的急性脑梗死患者７８例,随机分为蕲蛇酶配以高压氧治疗组（高压氧组）和蕲蛇酶治疗组（蕲蛇酶组）。结果 治疗前后两组总有效率分别为９４．７％和９２．５％。基本治愈、显著进步百分比是高压氧组高于蕲蛇酶组,但差异不显著（Ｐ〉０．０５）。神经功能缺损程度总分数治疗前后比较,蕲蛇酶配以高压氧组第１个疗程后,差异显著（Ｐ〈０．０５）,第２个疗程后,差异     

Role of lipid peroxidation in damage to serotonin receptors and development of epileptiform seizures during hyperoxia

Hyperoxia brought about substantial accumulation of primary and end products of lipid peroxidation (LPO) and a significant lowering of alpha-tocopherol content in rat brain tissues. Preinjection of animals with synthetic and natural antioxidants (4-methyl-2,6-ditretbutylphenol and alpha-tocopherol) prevented LPO activation and decreased the frequency of epileptiform seizures induced by hyperoxia. Administration of a mixture of unsaturated fatty acids led to an opposite effect. The changes in the properties of serotonin receptors were found to be dependent on the hyperoxia-induced LPO. These changes were marked by the reduced specific binding of serotonin with neuronal membranes of the rat brain cortex. The data obtained allowed the conclusion about the key role played by LPO activation in toxic action of hyperbaric activation on the brain.     

Combined use of hyperbaric oxygenation and antioxidants in the therapy of experimental myocardial infarct

In rabbits with experimental myocardial infarction, the combined use of hyperbaric oxygenation and ionol greatly potentiated the effect of the antioxidant on contractile function of the left ventricle, the time course of antioxidant lipid activity and superoxide dismutase activity of the myocardium.     

Effect of hyperbaric oxygenation on paramagnetic centers in the rabbit myocardium during experimental myocardial infarction

Changes in paramagnetic centres (PC) concentration in rabbit's myocardial muscle were studied under experimental myocardial infarction during 168 hours by means of ESR-spectroscopy. PC characterized by ESR signal with g = 3.0 was found. It was shown that hyperbaric oxygenation did not affect PC content in the infarction zone, and resulted in an increase of PC concentration with g = 1.94 and g = 2.0 in the intact myocardial zone.     

The effect of hyperbaric oxygenation on the antioxidant status of Xenopus laevis after its preliminary adaptation to oxygen]

We studied the level of lipid peroxidation and the activity of antioxidant enzymes (superoxide dismutase and catalase) in various tissues of adult Xenopus laevis after an initial exposure to hyperbaric oxygenation at the developmental stage 38. We have found that irrespective to the mode of treatment, the level of lipid peroxidation and activity of antioxidant enzymes in the brain, lungs, and blood of these animals were higher as compared to control animals. We demonstrate that, after the exposure of adult animals to hyperoxia, if they were earlier subjected to hyperbaric oxygenation (0.2 MPa) at stage 38, there was no intensification of lipid peroxidation or changes in the activity of superoxide dismutase and catalase. In adult animals initially subjected to hyperbaric oxygenation at the same stage of development but at the pressure--0.7 MPa, the second exposure to hyperoxia led to a drastic intensification of lipid peroxidation in the brain; in some animals, an increased level of lipid peroxidation products in the lungs was observed.     

SkQ1 Controls <Emphasis Type="Italic">CASP3</Emphasis> Gene Expression and Caspase-3-Like Activity in the Brain of Rats under Oxidative Stress

Here, we studied the effect of the mitochondria-targeted antioxidant SkQ1 (plastoquinone cationic derivative) on the CASP3 gene expression and caspase-3 activity in rat cerebral cortex and brain mitochondria under normal conditions and in oxidative stress induced by hyperbaric oxygenation (HBO). Under physiological conditions, SkQ1 administration (50 nmol/kg, 5 days) did not affect the CASP3 gene expression and caspase-3-like activity in the cortical cells, as well as caspase-3-like activity in brain mitochondria, but caused a moderate decrease in the content of primary products of lipid peroxidation (LPO) and an increase in the reduced glutathione (GSH) level. HBO-induced oxidative stress (0.5 MPa, 90 min) was accompanied by significant upregulation of CASP3 mRNA and caspase-3-like activity in the cerebral cortex, activation of the mitochondrial enzyme with simultaneous decrease in the GSH content, increase in the glutathione reductase activity, and stimulation of LPO. Administration of SkQ1 before the HBO session maintained the basal levels of the CASP3 gene expression and enzyme activity in the cerebral cortex cells and led to the normalization of caspase-3-like activity and redox parameters in brain mitochondria. We hypothesize that SkQ1 protects brain cells from the HBO-induced oxidative stress due to its antioxidant activity and stimulation of antiapoptotic mechanisms.     

Effect of hyperbaric oxygenation on the Na+, K+-ATPase and membrane fluidity of cerebrocortical membranes after experimental subarachnoid hemorrhage

It is reported that CNS hemorrage causes membrane dysfunction and may exacerbate this damage as a result of secondary ischemia or hypoxia. Since hyperbaric oxygenation improves oxygen metabolism, it may reduce this membrane damage. The present study was conducted to reveal whether hyperbaric oxygenation influences membrane alteration after hemorrhage. Thirty minutes after subarachnoid hemorrhage induction, rats were treated with hyperbaric oxygenation 2 ATA for 1 hour. Rats were decapitated 2 hours after subarachnoid hemorrhage induction. Na⁺, K⁺-ATPase activity measurement, and spin-label studies were performed on crude synpatosomal membranes. Subarachnoid hemorrhage decreased Na⁺, K⁺-ATPase activity. Spin label studies showed that hydrophobic portions of near the membrane surface became more rigid and the mobility of the membrane protein labeled sulfhydryl groups decreased after subarachnoid hemorrhage. Hyperbaric oxygenation significantly ameliorated most of the subarachnoid hemorrhage induced alterations. We conclude that hyperbaric oxygenation may be a beneficial treatment for acute subarachnoid hemorrhage.     

The effect of oxidative stress on nitrosomethylurea-induced mutagenesis in sunflower Helianthus annuus L

The effect of hyberbaric oxygenation on mutagenicity of nitrosomethylurea (NMU) was examined. It was shown that in the regimes studied, hyperbaric oxygenation enhances the NMU mutagenic effect both on the nuclear and on the plastid genetic material of sunflower, but do not increase intensity of free-radical reactions and do not induce plastid mutations and chromosome aberrations per se. At high concentrations inducing chromosome aberrations (0.03%), NMU was shown to enhance the level of free-radical processes. Possible mechanisms of the increase of NMU-induced mutagenesis by hyperbaric oxygenation are discussed.     

Hyperbaric oxygenation in the comprehensive rehabilitation of seamen after a long sea voyage]

It is established that 10 sessions of hyperbaric oxygenation in complex with balneologic procedures (Finnish baths) compensate the relative oxygen insufficiency and stimulate the redox processes of the sailor organism when transferring to a new functional level after long voyages. It is concluded that hyperbaric oxygenation is worth-while to restore working capacity and to rehabilitate the crews in the period after long sailing.     

Hyperbaric oxygen induces apoptosis via a mitochondrial mechanism

During therapeutic hyperbaric oxygenation lymphocytes are exposed to high partial pressures of oxygen. This study aimed to analyze the mechanism of apoptosis induction by hyperbaric oxygen. For intervals of 0.5–4 h Jurkat-T-cells were exposed to ambient air or oxygen atmospheres at 1–3 absolute atmospheres. Apoptosis was analyzed by phosphatidylserine externalization, caspase-3 activation and DNA-fragmentation using flow cytometry. Apoptosis was already induced after 30 min of hyperbaric oxygenation (HBO, P < 0.05). The death receptor Fas was downregulated. Inhibition of caspase-9 but not caspase-8 blocked apoptosis induction by HBO. Hyperbaric oxygen caused a loss of mitochondrial membrane potential and caspase-9 induction. The mitochondrial pro-survival protein Bcl-2 was upregulated, and antagonizing Bcl-2 function potentiated apoptosis induction by HBO. In conclusion, a single exposure to hyperbaric oxygenation induces lymphocyte apoptosis by a mitochondrial and not a Fas-related mechanism. Regulation of Fas and Bcl-2 may be regarded as protective measures of the cell in response to hyperbaric oxygen.     

Study of bromthymol blue-prealbumin in the blood serum of rats under hyperbaric oxygenation]

Three-fold increase of BTB-prealbumin (Rm 1.0) in rat serum following fierse convulsions under hyperbaric oxygenation (6 ati, 30-35 min) has been proved by disc electrophoresis. Glial S100-protein and 7-fold increase in the all-organ component of brain BTB-prealbumin were found by immunochemistry to appear in the serum of experimental rats. The consequences of disorders in the blood-brain barrier for non-specific, all-organ proteins and potentialities of protein output from the brain into the blood similarly to neurophysins under hyperbaric oxygenation are discussed.     

The Influence of Hyperbaric Oxygenation (HBO) on Proliferation and Differentiation of Human Keratinocyte Cultures In Vitro

A drop in tissue oxygen partial pressure below 30mm Hg as a result of reduced perfusion in an extensive area of acute skin damage, or where a large number of chronic skin defects occur, inhibits collagen synthesis and neoangiogenesis in the various phases of wound healing. Subsequent granulation and epithelialisation are correspondingly impaired.Hyperbaric oxygenation is now recognised as a valuable supplementary method of treatment for problematic wounds. Stimulation of fibroblast and endothelial cell proliferation through Hyperbaric oxygenation has been demonstrated in numerous studies.The aim of this study was to investigate the effect of hyperbaric oxygen treatment on the proliferation and differentiation of human keratinocyte cultures.The influence of hyperbaric oxygenation on the proliferation of human keratinocyte cultures was demonstrated using flow-through cytometry and a fluorescence activated cell sorter, which detects fluorescence intensity following incorporation of 5-bromo-2-deoxyuridine in cell DNA.The degree of cell differentiation was deduced from the expression of various components of the cytoskeleton, such as cytokeratin 10 and involukrin, the production of which was quantified through the determination of monoclonal antibodies against cytokeratin 10 and involukrin from measurements of fluorescence activity in a flow-through cytometer.Hyperbaric oxygenation of cell cultures in vitro did not produce a significantly higher rate of cell proliferation, so that no increase in vitality was observed.An interesting observation following exposure to hyperbaric oxygen was the marked increase in expression of both cytokeratin 10 and involukrin, as an indication of accelerated cell differentiation.     

Suppression of humoral antibody synthesis on exposure to hyperbaric oxygenation

The influence of hyperbaric oxygenation (HBO) on the immune response in mice, immunized intraperitoneally with sheep red blood cells, was studied. HBO was shown to reduce hemagglutinin and hemolysin titres in peripheral blood as well as to decrease the amount of antibody-forming cells in the spleen. The most pronounced immunodepressant HBO effect is seen when hyperbaric oxygenation is carried out under toxic conditions before immunization of the animals with low antigen doses. Relationship is shown between the immunodepressant HBO effect and reduced leucocyte and lymphocyte counts in peripheral blood of the animals.     

The effect of oxidative stress on nitrosomethylurea-induced mutagenesis in sunflower <Emphasis Type="Italic">Helianthus annuus</Emphasis> L.

The effect of hyberbaric oxygenation on mutagenicity of nitrosomethylurea (NMU) was examined. It was shown that in the regimes studied, hyperbaric oxygenation enhances the NMU mutagenic effect on the plastid genetic material of sunflower. Possible mechanisms of the increase of NMU-induced mutagenesis by hyperbaric oxygenation are discussed.Translated from Genetika, Vol. 41, No. 1, 2005, pp. 63–70.Original Russian Text Copyright © 2005 by Usatov, Mashkina, Guskov.     

Expanding the limits of composite grafting: a case report of successful nose replantation assisted by hyperbaric oxygen therapy

A successful nose replantation assisted by hyperbaric oxygen therapy is presented, with a brief discussion of the possible mechanisms and a brief literature review of the use of hyperbaric oxygen in tissue preservation and replantation. Although it is not certain that the hyperbaric oxygenation ensured the survival of the replanted nose in this 2-year-old girl, there was documented change in graft appearance during the initial hyperbaric oxygen treatment. A 1-month, 1-year, and 2-year follow-up is included.     

Structural changes in the lungs induced by different levels of hyperbaric oxygenation

Morphological and ultrastructural changes in the lungs of 30 rabbits placed into the altitude chamber with 100% O2 and the pressure of 2, 2.5, 3 and 4 ata for 60 min daily during 1, 2 and 3 weeks have been studied. Morphological changes in the lungs were shown to depend on the degree and duration of oxygen pressure. 2 ata for 60 min daily during two weeks or 2.5 ata for 60 min daily during one week were considered to be safe regimens of hyperbaric oxygenation. Microcirculatory disorders and dystrophic changes of the aero-hematogenic barrier (AHB), its increased permeability, the development of intraalveolar and interstitial edema are observed in the lungs at a higher pressure of 3 or 4 ata. The endothelium and type I alveolocytes are more sensible to high doses of hyperbaric oxygenation. Hydropic degeneration and exfoliation of cells from the basilar membrane are gradually increasing. Type II alveolocytes are more stable to the destructive action of hyperbaric oxygenation. Greater dystrophic changes in other AHB elements are associated with the hypertrophy of mitochondria and lamellar bodies. The described AHB changes are more expressed in atelectasis areas.     

Dynamics of the plastic processes in the liver during the use of hyperbaric oxygenation in the recovery period following acute massive blood loss

Acute massive loss of blood lethal for most white rats was induced by blood-letting from the jugular vein (3.5% of the animal mass). The use of hyperbaric oxygenation at 3 atmos (3039 h Pa) immediately after blood-letting for 60 min prevented the depression of RNA and protein synthesis in the liver and the agony development in animals. Daily use of hyperbaric oxygenation during 2 weeks at the oxygen pressure of 3 to 0.5 atmos (3039-506 h Pa) had a stimulating effect on the reparative plastic processes in the liver, increased the survival rate in animals, and shortened the rehabilitation period.     

Effect of the hyperbaric oxygenation of animals and man on mitochondrial function in their tissues (based on EPR study data)

The ration of differential intensities of EPR signal of free endogenous radicals of semiquinone type and iron-sulfur proteins recorded at the temperature of liquid nitrogen in tissues (R index) is proposed as a criterion for estimation of changes in the functional state of mitochondria in human and animal tissues treated with hyperbaric oxygenation (HBO). The increase in R value was observed in hearts of intact mice and rabbits treated with HBO in near-toxic doses. This indicates a shift in mitochondria redox state towards oxidation. The above effect was not observed in mitochondria from intact zone of myocardium in animals with experimental infarction, and the numbers of mitochondria in the tissue increased after HBO. HBO treatment of women with pathological pregnancy leads to the decrease in R value for placental mitochondria.     

Effect of hyperbaric oxygenation on the course of experimental staphylococcal infection and on the immune status of the animal body

In guinea pigs infected with staphylococci by subcutaneous injection a decreased content of T-lymphocytes, an increased number of B-lymphocytes and lower levels of lysozyme and complement were observed. When subjected to the action of hyperbaric oxygenation, the animals, both intact or infected with staphylococci, showed the aggravation of staphylococcal infection, a decrease in the number of T-lymphocytes and an increase in the content of B-lymphocytes. In the intact animals hyperbaric oxygenation stimulated the production of complement and lysozyme, produced a decrease in the number of T-lymphocytes and an increase in the number of B-lymphocytes.     

Limitation of ischemic necrosis by the use of antioxidant ionol

Inhibitory effect of Ionol on lipid peroxidation (LPO) in the infarction zone and out of it after experimental myocardial infarction in the experiments on rats was investigated. The results of measurements, performed by two independent methods: point counting and the computer image analysis were compared. It was shown that LPO activation out of the ischaemic zone was prevented and dimensions of the ischaemic necrosis were limited by Ionol, which did not influence LPO activation in the ischaemic zone. Data obtained by both methods coincide qualitatively, the computer image analysis being more sensitive and effective.