Reaction of rats to the effect of hyperbaric oxygenation after preliminary adaptation to hypoxia

Preliminary adaptation of rats to hypoxia in the regimen exceeding the resistance to many stress agents not only produced no protective effect in response to the action of increased oxygen pressure (IOP) up to 6 kg/cm2, but, on the contrary, decreased the organism resistance. Thus, the time of occurrence of convulsions in the adapted rats was shortened, particularly when IOP acted 24 or 48 hours after the termination of training to hypoxia; this effect was somewhat weaker in experiments conducted in 3 to 4 days. Reactions became completely normal one month after the termination of training to hypoxia. Possible causes of the phenomena detected are discussed.     

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.     

Heparin effects during hyperbaric oxygenation in rats

The effects of heparin were studied concurrently with development of neurological and respiratory signs of oxygen toxicity in awake unrestrained rats exposed to 3 atmosphere absolute (ATA) oxygen. The modification of the early electrophysiological manifestations of CNS oxygen toxicity by heparin in the absence of obvious signs of pulmonary oxygen toxicity was also determined at 5 ATA oxygen by electrocorticographic recording. The femoral artery of all rats was cannulated two days before the exposures to hyperbaric oxygenation (HBO), and the effect of intraarterial injection of 10 U/100g/3h heparin or an equivalent volume of saline was studied in experimental and control rats, respectively. In rats exposed to 3 ATA oxygen, the latency of the onset of the first oxygen-induced convulsions, the time interval between the first convulsion and death, and the survival time were measured. Exposure to 5 ATA oxygen was continued until the onset of the first preconvulsive paroxysmal electrical discharges (FED), considered to be an early electrophysiological indicator of CNS oxygen toxicity. The onset of convulsions was slightly delayed in heparin-treated rats exposed to 3 ATA oxygen, and the time interval between the first convulsions and death was significantly reduced in heparinized rats. No difference in survival time between heparin- and saline-treated rats was observed. Heparin significantly delayed the time of onset of the FED during exposure to 5 ATA oxygen. Gross postmortem examination of the lungs and internal organs revealed only a bloody froth in the trachea of the heparin-treated rats exposed to 3 ATA oxygen. It is concluded that the heparin-hyperoxic interaction during development of pulmonary and CNS oxygen toxicity may be related to the anticoagulant effect of heparin and hyperoxic-induced pulmonary lesions.     

Lipid peroxidation in experimental myocardial infarct: the action of hyperbaric oxygenation

Rats with experimental myocardial infarction demonstrated decrease in the activity of superoxide dismutase and catalase and increase in the content of lipid peroxidation (LPO) products and Schiff bases both in and outside the area of necrosis. The combined ischemic damage and hyperbaric oxygenation resulted in the over additive effect of accumulation of LPO products in and outside the area of infarction. The data suggest that it is desirable to use antioxidants during hyperbaric oxygenation.     

The ceruloplasmin-transferrin antioxidant system during hyperbaric oxygenation in rats

Antioxidant system ceruloplasmin-transferrin (Cp-Tr) and malonic dialdehyde (MDA) concentration changes were studied in the rat serum after the exposure to hyperbaric oxygenation (HBO) at 4 atm for 25 min. 5 sessions of HBO led to an increase in serum MDA concentration. 5 HBO sessions were followed by the activation of Cp-Tr system. Afterwards MDA concentration began to decrease and by the 9th session even reached the initial levels. It is suggested that antioxidant system Cp-Tr takes part in the protection of the organism from toxic oxygen action.     

Conjugated dinitrocompound dianions as inhibitors of the oxidative deamination of monoamines

The conjugated derivatives--1.4-dinitrobutene-2, 1,4-dinitro-2-methylbutene-2, 1,4-dinitro-2,3-diphenylbutene-2 sodium salts, as well as dinitromethane sodium salt and beta-nitrostyrol, the inhibitors of oxidative deamination of serotonin, tyramine, tryptamine and benzylamine in bovine liver mitochondria, were studied. All the derivatives under study were found to be active inhibitors of monoamine oxidase catalyzing the oxidative deamination of serotonin, tyramine and tryptamine. In a far lesser degree these preparations inhibited the deamination of benzylamine, a specific substrate for monoamine oxidase B. All the dinitrocompound dianions, with the exception of 1,4-dinitro-2,3-diphenylbutene-2 disodium salt, a non-competitive inhibitor of oxidative deamination of the four substrates under study, cause competitive reversible inhibition of monoamine oxidase.     

Spermine and spermidine polyamines in the brain and liver of rats under hyperoxic action

The effect of hyperbaric oxygenation (6 atmospheres) on the content of polyamines spermine and spermidine in the rat brain and liver was studied. A decrease of the spermidine content in the brain and liver during oxygen convulsions and four hours after decompression was revealed. The spermine content in the brain during oxygen convulsions decreased as well, but four hours after decompression it increased significantly not eaching the control level. The spermine content in the liver failed to alter during oxygen convulsions, but the next four hours rose sharply. The role of polyamines in the regulation of protein biosynthetic processes under hyperoxia is discussed.     

Iron-containing proteins and the proteolytic activity in the blood serum in hyperbaric oxygenation and the protective action of urea

The number and composition of ferro-containing proteins, the total number of iron, summary peroxidase activity and peptide-hydrolase activity have been determined under different hyperbaro-oxygenation (HBO) in blood serum. It has been established that under HBO the concentration of ferro-containing proteins increases, the fraction composition of serum and erythrocyte haemoglobin changes, the activity of acid peptide-hydrolases increases and the protamine-splitting peptide-hydrolase activity lowers. The administration of urea before HBO-experiments leads to the normalization of the most biochemical indicators of blood serum. The tests of oxygen intoxication depth assessment have been suggested.     

Peptide hydrolase activity of blood serum, myocardium and skeletal muscles of rats under different states of hyperbaric oxygenation

Intensity of autolysis and proteolysis (hemoglobin as a substrate) of blood serum, myocardium and skeletal muscles was determined under normal conditions and under the effect of 2.0, 3.5 at. abs. of oxygen for 60 min and 5 at. abs. for 10 and 60 min. Under the effect of 3.5 and 5 at. abs. of oxygen there occurs a considerable increase in a degree of autolysis and proteolysis of the studied tissues as compared to the effect of 2 at. abs. of oxygen. But. these changes are not specific for the oxygen toxic doses.     

Study of rat erythrocyte superoxide dismutase activity during a toxic regimen of interrupted hyperbaric oxygenation]

Development of toxic manifestations in rats under conditions of hyperoxia was accompanied by a significant lowering of the rat erythrocyte superoxide dismutase activity. The incubation of control rats hemolysate with hydrogen peroxide (10(-3)M) or with kumole peroxide (1.6 10(-4)M) also led to pronounced fall of the initial erythrocyte superoxide dismutase activity. As supposed, the lowering of the erythrocyte superoxide dismutase activity under hyperoxia could be due to the formation of peroxidation products.