中华神经医学杂志
中華神經醫學雜誌
중화신경의학잡지
CHINESE JOURNAL OF NEUROMEDICINE
2008年
7期
684-687,697
,共5页
柯齐斌%江娅%孙德海%李庆华%葛广凤
柯齊斌%江婭%孫德海%李慶華%葛廣鳳
가제빈%강아%손덕해%리경화%갈엄봉
缺血预处理%长托宁%脊髓%缺血再灌注损伤
缺血預處理%長託寧%脊髓%缺血再灌註損傷
결혈예처리%장탁저%척수%결혈재관주손상
Ischemic preconditioning%Penehyclidine hydrochloride%Spinal cord%Ischemia-repeffusion injury
目的 探讨缺血预处理和长托宁对脊髓缺血再灌注损伤的防治作用及其可能的作用机制.方法 家兔24只按随机数字表法分为假手术组(A组)、缺血再灌注组(B组)及缺血预处理(IPC)和长托宁治疗组(C组).B、C组阻断腹主动脉40min,再灌注7d.C组IPC 5min,再灌注30min,再灌注20 min时静注长托宁0.2 mg/kg.分别测定阻断前10 min(C-10)、开放前即刻(C40)、再灌注60min(R60)7d(R7d)血清丙二醛(MDA)、超氧化物歧化酶(SOD)、肌酸激酶(CK)、肌酸激酶脑型同工酶(CK-BB);观察术后后肢神经功能;镜下脊髓病理学观察;计数脊髓凋亡神经元.结果 缺血再灌注后B组MDA、CK、CK.BB值明显高于C-10及A组相应时点值(P<0.05或P<0.01),SOD值变化同MDA变化相反;C组MDA、CK、CK-BB值明显高于C-10值(p<0.05),但明显低于B组相对应时点值(P<0.01),差异有统计学意义,但较A组差异无统计学意义.B组凋亡细胞数明显多于A组;C组明显少于B组,但多于A组,差异有统计学意义(P均<0.01).C组瘫痪发生率明显低于B组,其后肢神经功能明显好于B组.差异有统计学意义(P均<0.01).C组脊髓病理变化明显轻于B组.结论 IPC和长托宁对脊髓缺血再灌注损伤有良好的防治作用,其机制可能与其抗氧化反应及防治脊髓细胞损伤作用有关.
目的 探討缺血預處理和長託寧對脊髓缺血再灌註損傷的防治作用及其可能的作用機製.方法 傢兔24隻按隨機數字錶法分為假手術組(A組)、缺血再灌註組(B組)及缺血預處理(IPC)和長託寧治療組(C組).B、C組阻斷腹主動脈40min,再灌註7d.C組IPC 5min,再灌註30min,再灌註20 min時靜註長託寧0.2 mg/kg.分彆測定阻斷前10 min(C-10)、開放前即刻(C40)、再灌註60min(R60)7d(R7d)血清丙二醛(MDA)、超氧化物歧化酶(SOD)、肌痠激酶(CK)、肌痠激酶腦型同工酶(CK-BB);觀察術後後肢神經功能;鏡下脊髓病理學觀察;計數脊髓凋亡神經元.結果 缺血再灌註後B組MDA、CK、CK.BB值明顯高于C-10及A組相應時點值(P<0.05或P<0.01),SOD值變化同MDA變化相反;C組MDA、CK、CK-BB值明顯高于C-10值(p<0.05),但明顯低于B組相對應時點值(P<0.01),差異有統計學意義,但較A組差異無統計學意義.B組凋亡細胞數明顯多于A組;C組明顯少于B組,但多于A組,差異有統計學意義(P均<0.01).C組癱瘓髮生率明顯低于B組,其後肢神經功能明顯好于B組.差異有統計學意義(P均<0.01).C組脊髓病理變化明顯輕于B組.結論 IPC和長託寧對脊髓缺血再灌註損傷有良好的防治作用,其機製可能與其抗氧化反應及防治脊髓細胞損傷作用有關.
목적 탐토결혈예처리화장탁저대척수결혈재관주손상적방치작용급기가능적작용궤제.방법 가토24지안수궤수자표법분위가수술조(A조)、결혈재관주조(B조)급결혈예처리(IPC)화장탁저치료조(C조).B、C조조단복주동맥40min,재관주7d.C조IPC 5min,재관주30min,재관주20 min시정주장탁저0.2 mg/kg.분별측정조단전10 min(C-10)、개방전즉각(C40)、재관주60min(R60)7d(R7d)혈청병이철(MDA)、초양화물기화매(SOD)、기산격매(CK)、기산격매뇌형동공매(CK-BB);관찰술후후지신경공능;경하척수병이학관찰;계수척수조망신경원.결과 결혈재관주후B조MDA、CK、CK.BB치명현고우C-10급A조상응시점치(P<0.05혹P<0.01),SOD치변화동MDA변화상반;C조MDA、CK、CK-BB치명현고우C-10치(p<0.05),단명현저우B조상대응시점치(P<0.01),차이유통계학의의,단교A조차이무통계학의의.B조조망세포수명현다우A조;C조명현소우B조,단다우A조,차이유통계학의의(P균<0.01).C조탄탄발생솔명현저우B조,기후지신경공능명현호우B조.차이유통계학의의(P균<0.01).C조척수병리변화명현경우B조.결론 IPC화장탁저대척수결혈재관주손상유량호적방치작용,기궤제가능여기항양화반응급방치척수세포손상작용유관.
Objective To investigate the protective effect of ischemic preconditioning (IPC) and penehyclidine hydrochloride (PHC) on the spinal cord against ischemia-reperfusion injury induced by aortic cross-clamping in rabbits. Methods Twenty-four rabbits were randomly divided into sham operation group (A), ischemia-reperfusion injury group (B) and IPC+PHC group (C). In group C, IPC was performed for 5 min, followed by reperfusion for 30 min, and PHC (0.2 mg/kg) was given at 20 min of rcperfusion. Then, in group B and C, the infrarenal aorta was clamped for 40 min followed by 7 d reperfusion. The aorta was not clamped in group A. The plasma concentrations of malondialdehede (MDA), superoxide dismutase (SOD), creatine kinase (CK) and creatine kinase BB isoenzyme (CK-BB) were assayed at 10 min before clamping, before unclamping, at 60 min and on the 7 th day after unclamping. After an operation, the neurological outcomes of the hind limbs were evaluated, the morphology of the spinal cord was observed, and the apoptotic spinal cord cells were measured by immunohistochemical technique. Results The concentrations of MDA, CK and CK-BB after ischemia-reperfusion in group B were increased significantly compared with those before clamping and those in group A (P<0.05 or 0.01); the concentrations in group C were higher than those before clamping (P<0.05), but lower significantly than those in group B (P<0.01), and not significantly different from those in group A. SOD was opposite. The apoptotic cells in group B were much more than that in groupA and in group C, but the number in group C was significantly higher than that in group A (P<0.01). The incidence rate of paralysis in group C was significantly lower than that in group B, and the neurological score of hinder limb was higher in group C than in group B (P<0.01). Pathological changes of the spinal cord was milder in group C than in group B. Conclusion The combination of IPC and PHC can protect the spinal cord from ischemia-reperfusion injury in rabbits; the main mechanism may be increasing antioxidant potential and preventing cell injury.