HYPERBARIC-OXYGEN AFTER GLOBAL CEREBRAL-ISCHEMIA IN RABBITS DOES NOT PROMOTE BRAIN LIPID-PEROXIDATION

Objective: To determine whether hyperbaric oxygen administered immedia tely after global cerebral ischemia increases free radical generation and lipid peroxidation in the brain or alters neurophysiologic recover y. Design: Prospective, randomized, controlled trial. Setting: Animal research laboratory. Subjects: Adult male New Zealand white rabbits. I nterventions: Anesthetized rabbits were subjected to 10 mins of global cerebral ischemia by infusing a mock cerebrospinal fluid into the sub arachnoid space and increasing intracranial pressure equal to mean art erial pressure. Immediately upon reperfusion, one group of rabbits (n = 9) was treated with hyperbaric oxygen at 2.8 atmospheres absolute fo r 75 mins while the control group (n = 9) breathed room air for an equ ivalent period of time, At the end of the reperfusion period, oxyradic al brain damage was determined by measuring brain levels of oxidized a nd total glutathione and free malondialdehyde. Neurophysiologic brain injury was assessed with cortical somatosensory evoked potentials. Mea surements and Main Results: Both oxidized glutathione and the ratio of oxidized glutathione to reduced glutathione (total minus oxidized) we re higher (p < .05) in the hyperbaric oxygen group, indicating that hy perbaric oxygen increased free radical generation. Nonetheless, brain malondialdehyde content, an index of lipid peroxidation, was similar ( p > .05) in the two groups, Cortical somatosensory evoked potential re covery at the end of reperfusion was 50% higher (p < .05) in the hyper baric oxygen-treated animals compared with controls. Conclusions: Trea tment with hyperbaric oxygen after ischemia increased the amount of ox ygen free radicals in the brain. However, this increase in free radica l generation was not associated with an increase in lipid peroxidation or a reduction in neurophysiologic recovery when measured after 75 mi ns of recirculation. These results suggest that hyperbaric oxygen admi nistered immediately after global ischemia does not promote early brai n injury.