ウサギ脊髄虚血モデルにおけるNMDA非競合的拮抗薬の効果-虚血後の神経学的徴候、細胞外液アミノ酸、CaM活性の変動による評価-

NMDA非竞争性拮抗剂对兔脊髓缺血模型的影响 - 通过缺血后神经体征、细胞外液氨基酸和 CaM 活性的变化进行评估 -

• 批准号: 07771046
• 负责人: 高木 伸之
• 金额: $ 0.7万
• 依托单位: Sapporo Medical University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Encouragement of Young Scientists (A)
• 财政年份: 1995
• 资助国家: 日本
• 起止时间: 1995 至 无数据
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-07771046/
• 关键词: Spinal cord ischemia; Aortic repair; Noncompetitive NMDA receptor antagonist; Dextrorphan; Microdialysis

胸部および胸腹部大動脈手術術中の脊髄虚血の結果起こる対麻痺は,現在でも重篤な合併症であり,いだま確実な保護法はない.N-methyl-D-aspartate(NMDA)型受容体に対する非競合的拮抗薬dextrorphan(DX)による脊髄保護効果を検討した.【研究方法】2.5〜3kg雄のNew Zealand white rabbitを使用し,腎動脈下大動脈を25分間単純遮断し脊髄虚血を作成した.遮断中の直腸温,食道温は37-39℃に維持した.実験群は、1群(n=10):生理食塩水投与,2群(n=9):DXを遮断前30分間で10mg/kgを静脈内投与し,遮断後は10mg/kg/hrで持続的静脈内投与,3群(n=6);遮断直後にDZ6mg/kgの動脈内投与とした.神経学的検討は,運動,知覚,膀胱直腸障害にて評価し,遮断解除後48時間まで行った.脊髄神経細胞の虚血変化の病理学的検討は,H-E染色,および抗microtubule associated protein 2抗体(MAP-2)を用いた免疫染色にて行った.また,脊髄前角での脊髄虚血後のアミノ酸濃度変化の検討は,microdialysis probeを用いて採取し,HPLCにて測定した.【成績】48時間後の運動,知覚の回復度は,ともに1群に比し2群(p<0.001),3群(p<0.05)で有意に高かった.また,2群では,膀胱直腸障害は1例も認めず,全例48時間後腰を上げることか可能であった.病理学的にも,MAP-2の免疫染色での反応神経細胞数は,1群に比し2群(p<0.01),3群(p<0.05)で有意に多く,虚血障害が抑制された.また,microdialysis法にて測定した脊髄細胞外液中の興奮性アミノ酸であるグルタミン酸とアスパラギン酸の濃度は,虚血により前者で10倍,後者で5倍と有意な(p<0.0001)増加を示した.【結論】興奮性アミノ酸の上昇は,遅発性神経細胞死を引き起こす一つの原因と考えられた.DXの虚血前,中の投与は,神経学的,病理学的にみて脊髄虚血に対し保護効果を示した.

During chest surgery and abdominal surgery, the results of chiropractic deficiency and hemoptysis resulted in severe concomitant symptoms. Make sure that the N-methyl-D-aspartate (NMDA) recipient is not a concomitant antagonist of dextrorphan (DX) chiropractic. [research methods] 2.5~3kg male New Zealand white rabbit is used to protect the disease. Cut off the deficiency of blood in the spine for 25 minutes during the exercise. The temperature of the esophagus was maintained at 37-39 ℃. Group 1 (n = 10), group 2 (n = 9), group 2 (n = 9), group 1 (n = 10), group 1 (n = 10), group 2 (n = 9), Theological exercise, exercise, knowledge, bladder barrier and bladder injury, 48 hours after the blockage is released. The histopathology was stained with Hmure E, and the anti-microtubule associated protein 2 antibody (MAP-2) was detected by immunostaining. In the anterior corner of the spine, after the deficiency of the spine, the temperature was changed. Microdialysis probe was used to pick up the temperature, and the HPLC was used to determine the temperature. 48 hours later, you know how to return to the temperature. Group 1 is better than group 2, and group 3 is intentionally high. The symptoms were mild in 2 groups, and straight bladder obstruction was found in 1 case. In all cases, the upper lumbar spine was abnormal after 48 hours. Pathological changes, MAP-2 immunostaining, cell count, group 1, group 2, group 3, deficiency and blood deficiency were more than those in group 2 and group 3, respectively. The method of microdialysts was used to determine the degree of acidity in the extracellular fluid of spinal cord, the former was 10 times of deficiency blood, the latter was 5 times of intention (p&lt). 0.0001) add the medicine to show the truth. [results] the cause of the disease is caused by the death of the child. Before the deficiency of blood, DX was given to the doctor, theology, pathology, spinal cord deficiency, blood deficiency, and protection.