Extension of brain tolerance to hyperbaric O2 by intermittent air breaks is related to the time of CBF increase

2006 ◽  
Vol 1084 (1) ◽  
pp. 196-201 ◽  
Author(s):  
Mikulas Chavko ◽  
Richard M. McCarron
Keyword(s):  
Hyperbaric O2

Major neurological events following foam sclerotherapy

2008 ◽  
Vol 23 (4) ◽  
pp. 189-192 ◽  
Author(s):  
R G Bush ◽  
M Derrick ◽  
D Manjoney
Keyword(s):  
Hyperbaric Oxygen ◽  
The Other ◽  
Neurologic Complications ◽  
Foam Sclerotherapy ◽  
Hyperbaric O2

Aim This report describes two complications of severe neurologic alterations (TIA, CVA) after foamed sclerotherapy injection. Methods Using foam sclerotherapy in accepted concentrations, volume, and in standard ratio of air to sclerosant, two serious neurologic complications occurred. Results In both cases described, unknown atrial communications existed resulting in foam emboli. One case involving the vertebral system resolved without treatment. The other involving the cerebral system was treated with hyperbaric oxygen. Conclusions Foam sclerotherapy can cause serious neurologic phenomenon even though the incidence is rarely described. Immediate treatment with 100% O2 and possible hyperbaric O2 therapy should be considered.

Mechanisms of protection against pulmonary hyperbaric O2 toxicity by intermittent air breaks

2007 ◽  
Vol 102 (5) ◽  
pp. 525-532 ◽  
Author(s):  
Mikulas Chavko ◽  
Richard T. Mahon ◽  
Richard M. McCarron
Keyword(s):  
Hyperbaric O2

Liposome-mediated augmentation of brain SOD and catalase inhibits CNS O2 toxicity

1984 ◽  
Vol 57 (6) ◽  
pp. 1674-1681 ◽  
Author(s):  
T. Yusa ◽  
J. D. Crapo ◽  
B. A. Freeman
Keyword(s):  
Central Nervous System ◽  
Superoxide Dismutase ◽  
Nervous System ◽  
Enzyme Activity ◽  
Intravenous Injection ◽  
Biological Effect ◽  
Central Nervous System Toxicity ◽  
Hyperbaric O2 ◽  
Dose Dependent ◽  
System Toxicity

Enzymes specific for O-2 and H2O2 metabolism [superoxide dismutase (SOD) and catalase] can be delivered to the rat brain following entrapment in liposomes and intravenous injection and will protect against hyperbaric O2-induced convulsions in rats. Liposome-mediated superoxide dismutase and catalase augmentation of brain enzyme activity was 2.7-fold and 1.9-fold, respectively, 15 min after intravenous injection of superoxide dismutase plus catalase-entrapped liposomes. Rats treated with liposomes containing superoxide dismutase plus catalase 2 h before 6 ATA 100% O2 exposure had the time to convulsion extended three times that of controls. This protective effect was dose-dependent and was primarily due to augmentation of catalase activity. These findings show O-2 and H2O2 are important mediators of hyperbaric O2-induced central nervous system toxicity and that liposome-mediated augmentation of brain antioxidant enzymes has a biological effect.

HYPERBARIC O2 FOR VERTIGO

1973 ◽  
Vol 73 (8) ◽  
pp. 1416-1438
Author(s):  
&NA;
Keyword(s):  
Hyperbaric O2

BCNU-induced protection from hyperbaric hyperoxia: role of glutathione metabolism

1988 ◽  
Vol 65 (6) ◽  
pp. 2531-2536 ◽  
Author(s):  
S. G. Jenkinson ◽  
J. M. Jordan ◽  
R. A. Lawrence
Keyword(s):  
Reductase Activity ◽  
Glutathione Metabolism ◽  
Hyperbaric Hyperoxia ◽  
Oxidation Reduction ◽  
Reduction Cycle ◽  
Hepatic Glutathione ◽  
Glutathione Oxidation ◽  
Glutathione Reductase Activity ◽  
Hyperbaric O2

To explore the role of the glutathione oxidation-reduction cycle in altering the sensitivity of rats to the effects of hyperbaric hyperoxia, we administered N,N-bis(2-chloroethyl)-N-nitrosourea (BCNU) to decrease tissue glutathione reductase activity. We then exposed these animals and their matched vehicle-treated controls to 100% O2 at 4 ATA. Animals that received BCNU and were immediately exposed to hyperbaric O2 showed enhanced toxicity by seizing earlier in the exposure than controls. Animals that received BCNU 18 h before the hyperbaric O2 exposure were paradoxically protected from the effects of the exposure with a prolongation of their time to initial seizure and a marked increase in their survival time during the exposure. Tissue glutathione concentrations were also measured in the various groups and the hyperbaric O2 exposure produced marked decreases in hepatic glutathione levels in all control animals. In animals treated with BCNU 18 h before exposure, hepatic glutathione concentrations also decreased, but the concentrations had significantly increased during the 18-h waiting period, allowing these animals to maintain hepatic levels in the normal range even during their hyperbaric exposures. We conclude that treatment of rats with BCNU 18 h before exposure to hyperbaric hyperoxia results in enhanced protection of the animals during the exposure.

Hyperoxic exposure affects the ventilatory response to hypoxia in awake rats

1988 ◽  
Vol 64 (1) ◽  
pp. 181-186 ◽  
Author(s):  
R. Arieli ◽  
D. Kerem ◽  
Y. Melamed
Keyword(s):  
Tidal Volume ◽  
Minute Ventilation ◽  
Whole Body ◽  
Hyperoxic Exposure ◽  
Ventilatory Parameters ◽  
Ventilatory Drive ◽  
Co2 Balance ◽  
Hyperbaric O2 ◽  
Hyperbaric Exposure ◽  
Ventilatory Response To Hypoxia

We tested whether hyperbaric O2 (HBO) has an adverse effect on the hypoxic ventilatory drive. Four groups of rats were exposed for 550 min to O2 at 1.67, 1.90, and 2.15 ATA and to air at 1.90 ATA, respectively. Ventilatory parameters (frequency, tidal volume, and minute ventilation) were measured using whole-body plethysmography, before the hyperbaric exposure, immediately after the exposure, and up to 20 days after the exposure. Resting ventilation was not affected after exposure at 1.90 ATA to air or at 1.67 ATA to O2. HBO at 1.90 and 2.15 ATA caused a reduction of frequency and an elevation of tidal volume at different inspired gases: air, 5% CO2 balance O2, 80% O2, and 4.5% O2. However, minute ventilation on the day after the hyperoxic exposure was not different from the control at either air, 5% CO2, or 80% O2 but was markedly attenuated on the first three breaths at 4.5% O2. The hypoxic ventilation decreased to 48 +/- 13 (SD) and 32 + 11% after 1.90 and 2.15 ATA, respectively. The ventilatory parameters recovered in the days after HBO. We conclude that HBO reversibly depresses the hypoxic ventilatory drive, most probably by a direct effect on the carotid O2 chemoreceptors.

Glucose metabolism in rat lung during exposure to hyperbaric O2

1979 ◽  
Vol 46 (5) ◽  
pp. 943-949 ◽  
Author(s):  
D. J. Bassett ◽  
A. B. Fisher
Keyword(s):  
Glucose Metabolism ◽  
Hyperbaric Oxygen ◽  
Glucose Utilization ◽  
Co2 Production ◽  
Rat Lung ◽  
Lung Metabolism ◽  
Rat Lungs ◽  
Atp Generation ◽  
Hyperbaric O2 ◽  
Stimulation Of

Lung metabolism on exposure to hyperbaric oxygen was studied in rat lungs perfused with artificial media and ventilated with O2 at 0.2, 1, or 5 ATA. During the first 80 min of exposure to O2 at 5 ATA, glucose utilization increased 55%, lactate plus pyruvate production increased 45%, total CO2 production increased 47%, tissue ATP decreased 17%, and the ATP/ADP decreased 29% compared with 0.2 ATA O2. The increased CO2 production was due to a nearly twofold stimulation of pentose cycle activity whereas mitochondrial CO2 production did not change significantly. There were no significant differences in metabolism between lungs studied at 0.2 and 1 ATA O2. During the next hour of perfusion, there was a marked increase in mitochondrial CO2 production of control lungs but tissue ATP/ADP did not change significantly. With oxygen at 5 ATA, mitochondrial CO2 production increased only slightly, tissue ATP/ADP decreased further, and lungs demonstrated accumulation of edema fluid. The results indicate that exposure of lungs to hyperbaric oxygen results in stimulation of NADPH turnover through the pentose cycle and increased ATP generation, although the increased rate was not sufficient to maintain normal ATP/ADP.

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