Effect of HBO on tissue PO2 in various organs

Central nervous system

Polarograhic measurements of tissue pO2 (PtiO2) in rat central nervous system (CNS)59 showed a range of 10-34mm Hg with normobaric air breathing. PtiO2 values rise to 452 ± 68mm Hg with breathing pure oxygen at 303.9kPa (3ata), and to 917 ± 123mm Hg with breathing pure oxygen at 506.5kPa (5ata) If CO2 is added to the inhaled gas, cortical pO2 increases even further because the vasoconstrictor response to hyperoxia is counteracted. With breathing a gas mixture of 95% O2 and 5% CO2, CNS PtiO2 increases to 791 ± 5mm Hg at 303.9kPa (3ata) and to 1540 ± 94mm Hg at 506.5kPa (5ata). Regional variations in PtiO2 depend on neuronal activity cerebral metabolic rate and blood flow. HBO decreases the concentration of NO which is a potent vasodilator, which provides protection against hyperoxic brain damage. In contrast, prolonged hyperoxia and/or higher levels of ambient pressure (506.5-607.8kPa, 5-6ata) led to increased NO production and blood flow, which could not be explained in detail.

Cerebral vasoconstriction, which is a determinant of tissue oxygen pressure, is the result of a sophisticated biochemical cascade of reactions in response to superoxide anion generation (O2-) induced by HBO. In this context, extracellular concentration of superoxide dismutase (SOD) plays a crucial role in regulating cerebral blood flow in vivo which could be shown in genetically altered mice strains60. High concentrations of SOD are found in vessels where NO is important for vascular relaxation.

Daugherty61 studied the effect of HBO at 1.5ata on cerebral PtiO2, oxygen consumption and mitochondrial function after lateral fluid-percussion injury in rats in comparison to 30% oxygen breathing. HBO was able to restore the reduced post-injury redox potential indicating impaired mitochondrial oxygen metabolism and to increase PtiO2 and brain VO2.

The impact of HBO on brain oxygenation at 192.5kPa (1.9ata) and 283.6kPa (2.8ata), intracranial pressure and brain glucose/ lactate levels was determined in anaesthetized and ventilated non brain injured pigs62. A normobaric increase of the FiO2 from 0.4 to 1.0 resulted in a rise of brain PtiO2 from 33 ± 14 to 63 ± 28mm Hg. A further increase was observed at 192.5kPa (1.9ata) (FIO2 of 1.0) to 151 ± 65mm Hg and at 283.6kPa (2.8ata) to 294 ± 134mm Hg. Intracranial pressure and glucose/lactate levels remained constant.

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