河南医科大学学报
河南醫科大學學報
하남의과대학학보
JOURNAL OF HENAN MEDICAL UNIVERSITY
2001年
1期
48-50
,共3页
消炎痛%兔%脑外伤%氧自由基%脑含水量
消炎痛%兔%腦外傷%氧自由基%腦含水量
소염통%토%뇌외상%양자유기%뇌함수량
目的：探讨消炎痛对急性实验性脑外伤后兔脑组织氧自由基反应的影响。方法：30只家兔随机分为A组(正常对照组)、B组(生理盐水治疗组)及C组(消炎痛治疗组)，每组10只动物。其中A组不致脑外伤，作为正常对照。B、C2组采用自由落体打击法建立兔闭合性脑外伤模型。C组于外伤后．10min开始，经耳缘静脉缓慢注入消炎痛针剂。B组于外伤后相同时间同样方法注入等量的生理盐水，作为生理盐水治疗对照。B、C2组于外伤后4h将动物处死，完整取出大脑半球以干湿重比较法测定大脑含水量；取挫伤灶周边脑组织制成匀浆，生化测定脑组织中过氧化物歧化酶(SOD)活性和脂质过氧化物(LPO)含量。结果：B组动物致脑外伤后4h，脑组织含水量及LPO含量分别为(79.918±1.449)％和(143.5±24.9)nmol／g，较对照组显著为高(P<0.01及P<0.05)，SOD活性为(1.97±0.16)Nu／mg，显著低于对照组(P<0.01)。C组应用消炎痛治疗后，脑组织含水量及LPO含量分别为(78.214±1．315)％和(118.1±13.7)nmol／g，与对照组比较，差异无显著性(P>0.05)；SOD活性为(2.25±0.21)Nu/mg，较B组明显升高(P<0．05)。结论：脑外伤早期应用消炎痛治疗，可减轻外伤脑组织中的氧自由基反应，保护血脑屏障，延缓并减轻脑水肿的形成和发展。
目的：探討消炎痛對急性實驗性腦外傷後兔腦組織氧自由基反應的影響。方法：30隻傢兔隨機分為A組(正常對照組)、B組(生理鹽水治療組)及C組(消炎痛治療組)，每組10隻動物。其中A組不緻腦外傷，作為正常對照。B、C2組採用自由落體打擊法建立兔閉閤性腦外傷模型。C組于外傷後．10min開始，經耳緣靜脈緩慢註入消炎痛針劑。B組于外傷後相同時間同樣方法註入等量的生理鹽水，作為生理鹽水治療對照。B、C2組于外傷後4h將動物處死，完整取齣大腦半毬以榦濕重比較法測定大腦含水量；取挫傷竈週邊腦組織製成勻漿，生化測定腦組織中過氧化物歧化酶(SOD)活性和脂質過氧化物(LPO)含量。結果：B組動物緻腦外傷後4h，腦組織含水量及LPO含量分彆為(79.918±1.449)％和(143.5±24.9)nmol／g，較對照組顯著為高(P<0.01及P<0.05)，SOD活性為(1.97±0.16)Nu／mg，顯著低于對照組(P<0.01)。C組應用消炎痛治療後，腦組織含水量及LPO含量分彆為(78.214±1．315)％和(118.1±13.7)nmol／g，與對照組比較，差異無顯著性(P>0.05)；SOD活性為(2.25±0.21)Nu/mg，較B組明顯升高(P<0．05)。結論：腦外傷早期應用消炎痛治療，可減輕外傷腦組織中的氧自由基反應，保護血腦屏障，延緩併減輕腦水腫的形成和髮展。
목적：탐토소염통대급성실험성뇌외상후토뇌조직양자유기반응적영향。방법：30지가토수궤분위A조(정상대조조)、B조(생리염수치료조)급C조(소염통치료조)，매조10지동물。기중A조불치뇌외상，작위정상대조。B、C2조채용자유락체타격법건립토폐합성뇌외상모형。C조우외상후．10min개시，경이연정맥완만주입소염통침제。B조우외상후상동시간동양방법주입등량적생리염수，작위생리염수치료대조。B、C2조우외상후4h장동물처사，완정취출대뇌반구이간습중비교법측정대뇌함수량；취좌상조주변뇌조직제성균장，생화측정뇌조직중과양화물기화매(SOD)활성화지질과양화물(LPO)함량。결과：B조동물치뇌외상후4h，뇌조직함수량급LPO함량분별위(79.918±1.449)％화(143.5±24.9)nmol／g，교대조조현저위고(P<0.01급P<0.05)，SOD활성위(1.97±0.16)Nu／mg，현저저우대조조(P<0.01)。C조응용소염통치료후，뇌조직함수량급LPO함량분별위(78.214±1．315)％화(118.1±13.7)nmol／g，여대조조비교，차이무현저성(P>0.05)；SOD활성위(2.25±0.21)Nu/mg，교B조명현승고(P<0．05)。결론：뇌외상조기응용소염통치료，가감경외상뇌조직중적양자유기반응，보호혈뇌병장，연완병감경뇌수종적형성화발전。
To investigate the effects of indomethacin(IM) on free radicalreactions in brain tissues of rabbits with acuteexperimental brain injury. Methods: Thirty rabbits were divided into thee groups randomly(ten animals in each group). Group A: the normal control group. Group B: the control group treated with saline. Group C: the group treated with IM. The animals in groupA were not hit. To establish the acute closed brain injury model, the animals of B and C groups were hit by a free falling object. Atthel0th minute after brain injury,the animals in group B and C were injected with normal saline and IM 4 mg/kg respectively atthe fnst time through the ear edging vein. To evaluate SOD activity, LPO and water content in brain tissues, the animals werekilled and their brains were fetched out intactly at four hours after brain injury. Results: The water content and content of LPO inbrain tissues of group B animals were (79. 918 + 1. 449)% and (143.5 + 24.9)nmol/g respectively, which were significantlyhigher than those of the normal control group ( P < 0.01, P < 0.05), and the activity of SOD was ( 1.97 + 0.16) Nu/mg, signifi-cantly lower than that in the control group C ( P < 0.01).After treatment with lM,the values of water and LPO content in groupanimals were (78.214 + 1.315) % and (118.1 + 13.7)nmol/g respectively, no significance was found between group C and groupA ( P > 0.05). The mean value of SOD activity was (2.25 + 0.21 ) Nu/mg, higher than that in group B ( P < 0.05). Conclusion:IM treatment at the early stage of brain injury could attenuate oxygen free radical reaction in injured brain tissues, protect bloodbrain barrier, prevent traumatic cerebral edema being formed and developing fmther.
