The effect of thyrotropin releasing hormone on carbon dioxide laser induced lesion of the cerebral artery

PubMedID: 9090641Carbon dioxide laser which is used widely in neurosurgery has less traumatic effect on the tissue beside the lesion than other types of laser. There has been little study on the changes to the vascular tissue, following laser application. We performed a study on 4 groups of dogs; comprising craniectomy only, craniectomy and thyrotropin releasing hormone (TRH), craniectomy and laser, and craniectomy, laser and TRH. We applied CO2 laser on the angular artery of two groups of dogs. To one group we infused TRH for 15 days following the laser application and to the other group we did not. We investigated the ultrastructural and biochemical changes and the effect of TRH on the tissue 15 days following laser application. In our study, we observed an increase in superoxide dismutase activity and a decrease in ATP- ase activities in the degenerated tissue on which CO2 laser was applied. TRH partially prevented the vascular degeneration of CO2 laser but did not significantly change superoxide dismutase and Adenosine-5'-triphosphatase activities

Correlation of alterations on Na+-K+/Mg+2 ATPase activity, lipid peroxidation and ultrastructural findings following experimental spinal cord injury with and without intravenous methylprednisolone treatment

PubMedID: 7566528The sodium-potassium activated and magnesium dependent adenosine-5'-triphosphatase (Na+-K+/Mg+2 ATPase EC 3.6.1.3.) activity and lipid peroxidation and early ultrastructural findings are determined in rat spinal cord at the early stage of trauma produced by a surgical clip on the thoracal 2-7 segments. The effect of treatment with intravenous methylprednisolone (MP) was evaluated the basis of these biochemical alterations and ultrastructural findings in the same model. The specific activity of the membrane bound enzyme Na+-K+/Mg+2 ATPase was promptly reduced in as early as ten minutes following spinal cord injury and remained at a level lower than the levels in the control group and in the sham-operated group. Methylprednisolone treatment immediately after the trauma attenuated the inactivation of Na+-K+/Mg+2 ATPase. On the other hand, there was significant difference in lipid peroxide content between the sham-operated and the injured animals. Methylprednisolone treatment reduced thiobarbituric acid reactive substance (TBARS) content in Group IV. We determined a positive relationship among membrane-bound enzyme Na+ K+/Mg+2 ATPase activity, malondialdehyde (MDA) content and early ultrastructural changes in the traumatized and treated groups. These data provide evidence for a beneficial effect of methylprednisolone on the activation of Na+-K+/Mg+2 ATPase and lipid peroxidation and early ultrastructural changes in spinal cord injured rats. The possible mechanism of methylprednisolone effects on the membrane function and lipid peroxidation, and the correlation of biochemical changes with ultrastructural findings are briefly discussed. © 1995 Walter de Gruyter & Co

The Effects of the Pretreatment of Intravenous High Dose Methylprednisolone on Na+-K+/Mg+2 ATPase and Lipid Peroxidation and Early Ultrastructural Findings Following Middle Cerebral Artery Occlusion in the Rat

PubMedID: 8861704The sodium-potassium activated and magnesium dependent adenosine-5'-triphosphatase (Na+-K+/Mg+2 ATPase EC.3.6.1.3.) activity and lipid peroxidation and early ultrastructural findings were determined in rat brain at the acute stage of ischaemia produced by permanent unilateral occlusion of the middle cerebral artery (MCA). The effects of the pretreatment with intravenous high-dose methylprednisolone (MP) on these biochemical indices and ultrastructural findings were also evaluated in the same model. The rats were divided into four groups. In group I, 10 rats were used to determine Na+-K+/Mg+2 ATPase activity and the extent of lipid peroxidation by measuring the malondialdehyde (MDA) content and normal ultrastructural findings. In group II on 20 rats, only subtemporal craniectomy was done in order to determine the effects of the surgical procedure on these indices and findings. This group was treated intravenously with saline solution before occlusion. In group III with MCA occlusion, saline solution was administered intravenously to 20 rats in the same amount of methylprednisolone used in group IV, ten minutes before the occlusion. In Group IV, a single high-dose (30mg/kg) of methylprednisolone was administered intravenously, ten minutes before occlusion in 20 rats. After occlusion of the middle cerebral artery, Na+-K+/Mg+2 ATPase activity was decreased promptly in the first ten minutes in the ischaemic hemisphere and remained at a lower level than the contralateral hemispheres in the same group and the normal levels in group I, during 120 minutes of ischaemia. A single dose methylprednisolone pretreatment prohibited the inactivation of Na+-K+/Mg+2 ATPase. On the other hand, there was significant difference in malondialdehyde content between group I and group III. Malondialdehyde levels were significantly increased following ischaemia and a non-significant increase was observed in the contralateral hemisphere. Methylprednisolone treatment significantly decreased malondialdehyde content on the side of the ischaemic hemisphere. We conclude that there is a positive relationship between membrane-bound enzyme Na+-K+/Mg+2 ATPase activity, malondialdehyde content and early ultrastructural changes in the treated group with MP. These data suggest that the pretreatment injection of high doses (30 mg/kg) methylprednisolone contribute to the protection of the brain from ischaemia with stabilization of the cell membrane by effecting the lipid peroxidation and the activation of Na+-K+/Mg+2 ATPase