Imamura H
Department of Neurosurgery, Hokkaido University School of Medicine, Sapporo Japan.
Hokkaido Igaku Zasshi. 1994 Mar;69(2):236-47.
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.
本研究旨在证实大剂量甲基强的松龙治疗对创伤后脊髓缺血的保护作用。将17只体重215 - 330克的Wistar - King大鼠分为四组，即正常组（n = 5）、生理盐水治疗损伤组（对照组，n = 4）、30毫克/千克甲基强的松龙治疗组（n = 4）和60毫克/千克甲基强的松龙治疗组（n = 4）。动物吸入1.5%氟烷麻醉，在T7、8椎板切除术后于T7/8处进行硬膜外夹闭损伤（140克，持续3秒）。损伤后30分钟静脉注射总量为1毫升的生理盐水或甲基强的松龙，损伤后2小时使用14C - 碘安替比林放射自显影技术测量脊髓血流量（SCBF）。脊髓血流量的正常值为，灰质96.0±1.5毫升/100克/分钟（平均值±标准误），白质22.9±1.8毫升/100克/分钟。在灰质中，所有损伤组靠近损伤部位处的SCBF均严重下降，这三组之间无显著差异。在白质中，所有损伤组损伤部位的SCBF均下降，且无显著差异。在甲基强的松龙组中，从损伤部位的头端到尾端SCBF下降，但在生理盐水组中，在靠近损伤部位及损伤部位尾端超过3毫米处，SCBF下降程度不如甲基强的松龙组，且观察到SCBF增加（充血）。在所有损伤组中，白质SCBF在损伤部位头端而非尾端下降。损伤部位相邻白质的SCBF未下降，而是保持在正常范围内或略有充血。这些情况可能会导致相邻脊髓的继发性损伤。据认为，大剂量甲基强的松龙若对脊髓损伤有效，在急性期会抑制损伤部位相邻白质的SCBF，并防止继发性损伤的进展。
