An evaluation of the effectiveness of pre-ischemic hyperbaric oxygen and post-ischemic aminoguanidine in experimental cerebral ischemia.

OBJECTIVE: To study the effects of pre-ischemic hyperbaric oxygen (HBO) and post-ischemic aminoguanidine (AG) on the infarct volume in permanent middle cerebral artery occlusion. METHODS: This study was approved by the Animal Experiments Ethics Committee of Gulhane Military Medical Academy, Ankara, Turkey and carried out from March 2006 to August 2006. A total of 28 Sprague-Dawley rats (200-320 g) were divided into 4 groups: control (K) group (n = 7); HBO group (n = 7); HBO + AG group (n = 7); and the AG group (n = 7). All rats underwent middle cerebral artery occlusion (MCAO) by subtemporal craniectomy, and permanent ischemia was created. A 2.8 atmospheric pressure of HBO was first applied to the HBO and HBO + AG groups for 45 minutes, and occlusion was created after 2 hours. In the HBO + AG group, intraperitoneal administration of AG hemisulfate (100 mg/kg) was started 6 hours after MCAO, and was continued twice a day for 3 days. RESULTS: The rate of infarction was found to be 22.2+/-3.1% in the control group, 16.1+/-2.7% in the HBO group, 15.2+/-1.9% in the HBO+AG group, and 14.4+/-3.3% in the AG groups. The rate of infarctions (therefore the volume of infarct) in the HBO, HBO + AG, and AG groups were found to be significantly decreased compared with the control group (p=0.002, p=0.001, and p=0.001). CONCLUSION: In permanent MCAO-induced ischemia in rats, HBO and AG were observed to have a lowering effect on the infarct volume, but no additive effect was observed. This situation can be explained by different mechanisms of action.

Effects of methylprednisolone and hyperbaric oxygen on oxidative status after experimental spinal cord injury: a comparative study in rats.

The effects of hyperbaric oxygen (HBO) therapy or methylprednisolone on the oxidative status were evaluated in experimental spinal cord injury. Clip compression method was used to produce acute spinal cord injury rats. Hyperbaric oxygen was administered twice daily for a total of eight 90 min-sessions at 2.8 atmospheres. Methylprednisolone was first injected with a bolus of 30 mg/kg followed with an infusion rate of 5.4 mg/kg/h for 24 h. Five days after clip application animals were sacrificed and their traumatized spinal cord segment were excised. Tissue levels of thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were evaluated to reflect oxidant/antioxidant status. Non-treated clip-operated animals reflected significantly higher SOD, GSH-Px and TBARS levels that were found to be significantly higher than the sham-operated. Methylprednisolone was not able to lower these levels. HBO administration diminished all measured parameters significantly; however, their levels appeared already to be high when compared with sham animals. According to these results obtained on the 5th day after induction, HBO, but not methylprednisolone, seems to procure prevention against oxidative spinal cord injury.