Hyperbaric oxygen exposure does not result in oxidative damage to rabbit lung tissue

Introduction: Hyperbaric oxygen has several accepted medical indications. The advantages of high oxygen partial pressure must be weighed against the toxic effects of oxygen, primarily to the brain and lung. The objective of this study was to determine the degree of oxidative lung damage and the effects on antioxidants in a model of hyperbaric hyperoxia. We also sought to determine if the lung damage in animals exposed to these conditions would be altered by the approach to mechanical ventilation used. Methods: Eighteen New Zealand White rabbits were anesthetized and instrumented with tracheostomy and vascular catheters. Animals were assigned to one of three study groups. The first group received conventional mechanical ventilaton (CMV-2.4) in a hyperbaric chamber at 2.4 ATM with FiO2 of 1.0. The second group received partial liquid ventilation (PLV-2.4) with perflubron at FiO2 of 1.0 and 2.4 ATM and was otherwise treated identically. The third group served as controls (CMV-I) and received conventional mechanical ventilation at 1 ATM. All animals were ventilated for 4 hours before sacrifice. Longer exposure was not practical due to presumed CNS toxicity and subsequent hemodynamic instability despite effective gas exchange. To assess oxidant stress biochemically, we measured malondialdehyde an indication of lipid peroxidation of lung tissue. We also measured the concentration of reduced glutathione (GSH), and superoxide dismutase activity (SOD) with colorimetric assays. Results:*CMV-2.4 PLV-2.4 CMV-I MDA (nmol/g protein) 400 ± 91 324 ± 74 360 ± 77 GSH (nmol/g protein) 1063 ± 240 929 ± 268 836 ± 168 SOD (units/g protein) 3412 ± 636 3096 ± 1036 3154 ± 302 Values are means ± SD.*- indexed to grams of protein in lung homogenate Conclusions: These results indicate that exposure of rabbits to hyperbaric hyperoxia at FiO2 of 1.0 and 2.4 ATM for 4-hours does not cause oxidative damage to lipids in the lungs. This tolerance to oxygen toxicity cannot be explained by an increase in SOD activity nor a sacrifical reduction of glutathione.

Duke Scholars

Author Alexandre Tellechea Rotta Pediatrics, Critical Care Medicine