Mechanism of hyperbaric oxygen preconditioning-induced ischemic tolerance in spinal cord of rabbits

AIM To investigate the mechanism of hyperbaric oxygen (HBO) preconditioning induced ischemic tolerance in spinal cord. METHODS 21 male New Zealand white rabbits were randomly allocated to one of 3 groups (7 in each group): animals in control group received room air and normal ambient pressure (1 h·d -1 , 5 d); animals in HBO group received HBO pretreatment (100% O 2, 253.3 kPa, 1 h·d -1 , 5 d); DMTU group, animals received HBO pretreatment (100% O 2, 253.3 kPa, 1 h·d -1 , 5 d), but 500 mg·kg -1 dimethylthiourea (DMTU) was administered iv. 1 h before each HBO pretreatment. At 24 h after the last HBO pretreatment, the spinal cord ischemia was induced for 20 min by infrarenal aortic occlusion. At 48 h after reperfusion, the neurologic status was scored by the Tarlov criteria (in which 4 was normal and 0 was paraplegia). All the animals were sacrificed at 48 h after reperfusion and their spinal cords (L 5) were removed immediately for histopathologic examination. The malondialdehyde (MDA) levels in the animals of HBO and DMTU groups were measured at 24 h before HBO pretreatment, 1 h after each HBO treatment, 10 min before spinal cord ischemia and 10 min after reperfusion. RESULTS The neurologic function scores in HBO group were higher than that in Control and DMTU groups ( P 0.05) at 48 h after reperfusion. The number of normal motor neurons in the anterior spinal cord in HBO group was more than that in Control and DMTU groups ( P 0.05). There was no obvious change in MDA levels among different time points and between HBO and DMTU groups. CONCLUSION The mechanism of hyperbaric oxygen preconditioning induced ischemic tolerance in the spinal cord of rabbits might be related to the production of oxygen free radicals by HBO pretreatment.