大鼠全脑缺血再灌注时左旋四氢巴马汀对脑内离子稳态平衡的影响
대서전뇌결혈재관주시좌선사경파마정대뇌내리자은태평형적영향
Influence of L-tetrahydropalmatine on rat brain ion homeostasis in the course of cerebral ischemia reperfusion
  • 万方数据
    中国临床康复 중국림상강복
    CHINESE JOURNAL OF CLINICAL REHABILITATION
    2004年 13期 2561-2563 ,共3页

    杨光田%陈齐国

    양광전%진제국

    脑缺血再灌注%电解质%脑 腦缺血再灌註%電解質%腦
    뇌결혈재관주%전해질%뇌
    背景:脑缺血再灌注可使脑内离子稳态遭到严重破坏,这种离子稳态的破坏又可加重脑缺血再灌注损伤.目的:通过观察脑缺血再灌注时脑组织钙、镁、锌、钠、钾、铁含量的变化,探讨左旋四氢巴马丁在全脑缺血再灌注损伤时的作用机制.设计:完全随机设计,对照实验研究.地点和材料:本研究的地点为华中科技大学同济医学院附属同济医院急诊科.材料由华中科技大学同济医学院实验动物中心提供清洁级Wistar大鼠35只,雌雄不拘,体重180～200 g,鼠龄4～6周.方法:建立大鼠急性脑缺血再灌注损伤模型,用原子分光光度仪检测脑组织电解质含量.结果:与假手术组比较脑缺血再灌注12 h组钙[(218.66±11.88)μg/g,q=5.526,P＜0.01]、锌[(72.45±0.830)μg/g,q=23.240,P＜0.01]、钠[(5 237.85±106.48)μg/g,q=7.956,P＜0.01]、钾[(15 421.52±264.86)μg/g,q=3.805,P＜0.05]、铁[(151.27±10.21)μg/g,q=3.392,P＜0.05]含量增高,镁[(617.71±13.91)μg/g,q=5.009,P＜0.01]含量降低;24 h钙[(295.63±64.69)μg/g,q=12.251,P＜0.01]、锌[(74.44±0.47)μg/g,q=27.354,P＜0.01]含量进一步增高,镁[(587.14±10.90)μg/g,q=10.499,P＜0.01]含量进一步降低,钠[(5 056.68±100.18)μg/g,q=5.269,P＜0.01]、钾[(15 116.52±631.96)μg/g,q=4.156,P＜0.05]含量仍升高,铁[(118.79±14.22)μg/g,q=2.515,P＞0.05]含量与假手术组接近.左旋四氢巴马丁在脑缺血再灌注12 h和24 h均能抑制脑组织钙[(175.67±2.70)μg/g,q=3.756,P＜0.05;(190.76±4.60)μg/g,q=9.163,P＜0.01]、锌[(66.77±1.14)μg/g,q=11.758,P＜0.01;(69.94±0.98)μg/g,q=9.304,P＜0.01]、钠[(4 841.94±179.00)μ.g/g,q=4.206,P＜0.05;(4 251.05±194.31)μg/g,q=3.183,P＞0.05]含量的上升,并提高脑组织镁[(706.21±25.92)μg/g,q=15.888,P＜0.01;(662.80±9.74)μg/g,q=13.585,P＜0.01]和钾[(16 294.68±102.48)μg/g,q=5.274,P＜0.01;(16 577.51±152.46)μg/g,q=3.339,P＞0.05]的含量,降低铁[(86.90±2.89)μg/g,q=11.607,P＜0.01;(84.85±3.21)μg/g,q=11.795,P＜0.01)含量.结论:左旋四氢巴马丁可抑制脑缺血再灌注期间脑组织钙、锌、钠含量的上升,提高镁和钾含量,降低铁含量.
    배경:뇌결혈재관주가사뇌내리자은태조도엄중파배,저충리자은태적파배우가가중뇌결혈재관주손상.목적:통과관찰뇌결혈재관주시뇌조직개、미、자、납、갑、철함량적변화,탐토좌선사경파마정재전뇌결혈재관주손상시적작용궤제.설계:완전수궤설계,대조실험연구.지점화재료:본연구적지점위화중과기대학동제의학원부속동제의원급진과.재료유화중과기대학동제의학원실험동물중심제공청길급Wistar대서35지,자웅불구,체중180～200 g,서령4～6주.방법:건립대서급성뇌결혈재관주손상모형,용원자분광광도의검측뇌조직전해질함량.결과:여가수술조비교뇌결혈재관주12 h조개[(218.66±11.88)μg/g,q=5.526,P＜0.01]、자[(72.45±0.830)μg/g,q=23.240,P＜0.01]、납[(5 237.85±106.48)μg/g,q=7.956,P＜0.01]、갑[(15 421.52±264.86)μg/g,q=3.805,P＜0.05]、철[(151.27±10.21)μg/g,q=3.392,P＜0.05]함량증고,미[(617.71±13.91)μg/g,q=5.009,P＜0.01]함량강저;24 h개[(295.63±64.69)μg/g,q=12.251,P＜0.01]、자[(74.44±0.47)μg/g,q=27.354,P＜0.01]함량진일보증고,미[(587.14±10.90)μg/g,q=10.499,P＜0.01]함량진일보강저,납[(5 056.68±100.18)μg/g,q=5.269,P＜0.01]、갑[(15 116.52±631.96)μg/g,q=4.156,P＜0.05]함량잉승고,철[(118.79±14.22)μg/g,q=2.515,P＞0.05]함량여가수술조접근.좌선사경파마정재뇌결혈재관주12 h화24 h균능억제뇌조직개[(175.67±2.70)μg/g,q=3.756,P＜0.05;(190.76±4.60)μg/g,q=9.163,P＜0.01]、자[(66.77±1.14)μg/g,q=11.758,P＜0.01;(69.94±0.98)μg/g,q=9.304,P＜0.01]、납[(4 841.94±179.00)μ.g/g,q=4.206,P＜0.05;(4 251.05±194.31)μg/g,q=3.183,P＞0.05]함량적상승,병제고뇌조직미[(706.21±25.92)μg/g,q=15.888,P＜0.01;(662.80±9.74)μg/g,q=13.585,P＜0.01]화갑[(16 294.68±102.48)μg/g,q=5.274,P＜0.01;(16 577.51±152.46)μg/g,q=3.339,P＞0.05]적함량,강저철[(86.90±2.89)μg/g,q=11.607,P＜0.01;(84.85±3.21)μg/g,q=11.795,P＜0.01)함량.결론:좌선사경파마정가억제뇌결혈재관주기간뇌조직개、자、납함량적상승,제고미화갑함량,강저철함량.
    BACKGROUND: Cerebral ischemia-reperfusion leads to disruption of brainion homeostasis that aggravates ischemia-reperfusion injury.OBJECTIVE: To investigate the action mechanism of L-tetrahydropalmatine(L-THP) in cerebral ischemia-reperfusion injury by observing the changes inthe contents of calcium, magnesium, zinc, sodium, potassium and iron in thebrain tissues.DESIGN: Completely randomized controlled study.SETTING and MATERIALS: This study was carried out in the EmergencyDepartment, Tongji Hospital, Huazhong University of Science and Technolo-gy. Thirty-five Wistar rats of clean grade weighing 180 - 200 g and aged 4 -6 weeks old were used.METHODS: Rat models of cerebral ischemia-reperfusion injury were estab-lished to determine the electrolyte contents using an atomic absorptionspectrophotometer ( AAS ).RESULTS: Compared with the sham operation group, the cerebral ischemia-reperfusion group, at 12 hours, had elevated levels of brain calcium[ (218.66 ±11.88) μg/g, q=5.526, P ＜0.01], zinc[(72.45±0.83) μg/g, q=23. 240, P ＜ 0.01 }, sodium[ (5 237.85 ± 106.48) μg/g, q = 7. 956, P ＜0.01], potassium[(15 421.52 ±264. 86) μg/g, q =3. 805, P ＜0.05] andiron[ (151.27 ± 10. 21 ) μg/g, q = 3. 392, P ＜ 0.05], but with lowered mag-nesium content; at 24 hours after the injury, further increases occurred in thelevels of calcium[(295. 63 ±64. 69) μg/g, q=12.251, P ＜0.01], zinc[(74.44±0.47) μg/g, q=27.354, P ＜0.01], sodium[ (5 056.68±100.18) μg/g, q=5.269, P ＜ 0.01] and potassium[(15 116.52±631.96) μg/g, q =4. 156, P ＜ 0. 05], while the content of magnesium[(587.14±10.90) μg/g, q=10.499, P ＜0.01] decreased, and thecontent of iron[(118. 79±14.22) μg/g, q=2.515, P＞ 0.05] wassimilar to that in the sham operation group. At both 12 and 24 hours after thereperfusion, L-THP inhibited the increase in the contents of calcium[ (175.67 ± 2.70) μg/g, q = 3. 756, P ＜ 0. 05; (190. 76 ± 4.60) μg/g,q=9.163, P ＜0.01], zinc[(66.77±1. 14) μg/g, q=11.758, P ＜0.01; (69.94 ± 0.98) μg/g, q = 9. 304, P ＜0.01] and sodium[ (4 841.94 ±179.00) μg/g, q=4.206, P ＜0.05; (4251.05±-194.31) μg/g, q=3. 183, P ＞ 0. 05], increased the contents of magnesium [ (706.21 ±-25.92) μg/g, q=15.888, P ＜ 0.01; (662.80±9.74) μg/g, q=13.585, P ＜0.01] and potassium[(16 294.68±102.48) μg/g, q=5. 274, P ＜ 0.01; (16 577.51 ± 152.46) μg/g, q = 3. 339, P ＞ 0.05], anddecreased the contents of iron[(86.90±2.89) μg/g, q=11.607, P ＜0.01;(84.85±3.21) μg/g, q=11.795, P ＜0.01].CONCLUSION: L-THP can inhibit the increase of calcium, zinc and sodiumcontents, increase the contents of magnesium and potassium, and decrease thecontent of iron in rat brain tissues during cerebral ischemia-reperfusion.`
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