The role of hyperbaric oksygen treatment in the experimental spinal injury model

After the spinal cord injury half of the patients can not return to their normal lives. It causes loss of work. Today we don?t have an effective treatment except metilprednisolon.Spinal cord injury has two mechanisms; mainly primary and secondary injuries. The first one causes necrosis and ends with the death of the cell. And the second one is the injury, that has started with the primary mechanism, and causes tissue damage with methabolic and biochemical pathways. The most important reason that starts the second mechanism is ischemia. Ischemia causes lack of energy. More clinical studies have showed that the injury is increased because of the secondary mechanisms.In our study we had five groups with total 40 animals. In the control group. only thoracal laminectomies were performed and no spinal cord injuries have been made. In the trauma group T9 total laminectomies were performed and spinal cord injuries were obtained with Tator method. In this group; no treatment options were used. Hyperbaric oksygen treatment were given at the 1. hour time point of spinal cord injury for the third group, at the 6. hour time point for the fourth group and at the 24. hour time point for the fifth group. The treatment was given at two cycles per day and the total treatment lasted for five days.In the theurotical basis of this study depends of this basic idea. In hiperbaric conditions when 100% of oxygen is inhalated, the amount of plasma oxygen increases. With the effect of high oxygen pressure the secondary spinal cord ischemia decreases.The motor strength of the animals tested in the 1., 3., and in the 5. days with inclined plane tests. Increases of the angles in the first group, that took HBO treatment in the first hour, had statistically significant results comparing to control group.The increases of motor strength in the first group, tested in the 1., 3. and 5. days, with Drumond Moore criterias had statistically significant results also.NO transforms immediately to NO2-(nitrite) with oxygen. In our study we compared the nitrite levels in spinal cord specimens with Griess reaction. There was a statistically significant difference between the trauma and the treatment group that took HBO in the first posttraumatic hour.In trauma group; macroscopical examinations of specimens showed tissue degradations and heavy heamorrhagic contusions mainly. In the group that treated with HBO; macroscopical examinations revealed less heamorrhagic areas and tissue damage. In the first hour posttraumatically HBO treated group III; showed only minimal heamorrhagic areas in where clips applied. In the groups that HBO treatments were performed after 6 and 24 hours posttraumatically, heamorrhagic areas were spreaded extensively comparing to HBO - 1 hour group.In the control group, the microscopical evaluation with hematoxylin and eosin showed normal neuronal and vasculer structures. In the trauma group the gray and white matter borders was not differentiated well. Great amount of haemorrhagic areas, and cavitation formation and liquefaction necrosis, oedema and leukocyte infiltration was seen. When these results compared with the sham group, there were significant quantitative differences. The group that took HBO in the first hour had clear border between gray and white matter areas with lesser heamorrhagic areas and less oedema. Histopathological findings of the groups that took HBO at the 6. and 24. hours time points had no big differences comparing with the trauma group.In our study; HBO treatment had showed statistically significant effects in terms of clinical, histopathological and biochemical parameters at the treatment of spinal cord injury comparing to control group.