[Effects of megadose methylprednisolone therapy on acute spinal cord injury in rats].
Present study was performed to confirm the protective effect of megadose methylprednisolone therapy for the posttraumatic spinal cord ischemia. Seventeen Wistar-King rats weighing 215-330 g were divided into four groups which were normal group (n = 5), injury group treated by saline (control group, n = 4), treated by methylprednisolone (MP) 30 mg/kg (n = 4) and treated by MP 60 mg/kg (n = 4). Animals were anesthetized aspirating 1.5% Halothane and made epidural clipping injury (140 g for 3 seconds) at Th7/8 after laminectomy of Th7,8. Saline or MP of which total volume was 1 ml was injected intravenously 30 minutes after injury and spinal cord blood flow (SCBF) was measured 2 hours after injury by using 14C-iodoantipyrine autoradiography technique. As for normal value of spinal cord blood flow, its gray matter is 96.0 +/- 1.5 ml/100 g/min (mean +/- SE), and white matter is 22.9 +/- 1.8 ml/100 g/min. In the gray matter, SCBF severely decreased in all injury groups as it closed to the injury site, and there was no significant difference among these three groups. In the white matter, SCBF decreased at the injury site in all injury groups and there was no significant difference. From rostral to caudal of the injury site SCBF decreased in MP groups, but in the saline group SCBF showed not so much decrease as MP groups at adjacent to the injury site and at more than 3 mm caudal to the injury site increase of SCBF (hyperemia) was observed. And decrease of white matter SCBF was observed in the rostral rather than in the caudal to the injury site in all injury groups. SCBF of the white matter adjacent to the injury site was not decreased, but preserved within normal range or rather slightly hyperemic. These condition may cause the secondary damage in the adjacent spinal cord. It is considered that megadose of methylprednisolone, if it is effective for the spinal cord injury, would suppress the SCBF of white matter of adjacent to the injury site at the acute phase and prevent the progression of secondary damage.
Imamura
H
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Department of Neurosurgery, Hokkaido University School of Medicine, Sapporo Japan.
D000208:Acute Disease; D000818:Animals; D000983:Antipyrine / Q000031:analogs & derivatives / Q000493:pharmacokinetics; D001345:Autoradiography; D002250:Carbon Radioisotopes / Q000493:pharmacokinetics; D008775:Methylprednisolone / Q000008:administration & dosage*; D051381:Rats; D017208:Rats, Wistar; D012039:Regional Blood Flow; D013116:Spinal Cord / Q000098:blood supply / Q000378:metabolism; D013119:Spinal Cord Injuries / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology
D002250:Carbon Radioisotopes; D000983:Antipyrine; C008135:iodoantipyrine; D008775:Methylprednisolone