创伤外科杂志
創傷外科雜誌
창상외과잡지
JOURNAL OF AUMATIC SURGERY
2013年
5期
436-439
,共4页
代文光%秦晓勇%李良慧%宋学良%冯玥%李臻
代文光%秦曉勇%李良慧%宋學良%馮玥%李臻
대문광%진효용%리량혜%송학량%풍모%리진
颅脑损伤%拮抗剂%线粒体%呼吸控制率%大鼠
顱腦損傷%拮抗劑%線粒體%呼吸控製率%大鼠
로뇌손상%길항제%선립체%호흡공제솔%대서
brain injury%antagonist%mitochondrion%respiratory control rate%rats
目的观察N-甲基-D-天门冬氨酸(N-mechy1 D-aspartate,NMDA)受体拮抗剂(MK-801液)对创伤后大鼠脑线粒体呼吸功能的影响,并探讨可能的作用机制,为临床应用MK-801治疗创伤性颅脑损伤提供依据。方法将Wistar大鼠80只随机分为4组:对照组20只,创伤未治组(非治疗组)20只,治疗24h组(治疗Ⅰ组)20只,治疗72h组(治疗Ⅱ组)20只。采用BIM-Ⅲ型小型多功能生物撞击机造成大鼠中型颅脑损伤,用氧电极法分析线粒体呼吸功能(呼吸Ⅲ、Ⅳ态和呼吸控制率),并行透视电镜观察线粒体超微结构。结果(1)与对照组比较,非治疗组伤后72h呼吸Ⅲ态和呼吸控制率明显下降;治疗Ⅰ组呼吸功能有所恢复;治疗Ⅱ组呼吸Ⅲ态和呼吸控制率较治疗疗Ⅰ组有显著升高(P<0.05),呼吸Ⅳ态稍有延长,但相差不显著。(2)与对照组比较,电镜结果示伤后非治疗组与治疗Ⅰ组、Ⅱ组线粒体结构均有不同程度的损害,但治疗Ⅰ组、Ⅱ组线粒体损害程度减轻。结论创伤性颅脑损伤后脑线粒体呼吸功能明显下降。应用MK-801治疗颅脑损伤大鼠可明显改善脑线粒体呼吸功能,电镜观察也发现线粒体超微结构损害程度减轻。治疗时间越长,呼吸功能改善越明显。
目的觀察N-甲基-D-天門鼕氨痠(N-mechy1 D-aspartate,NMDA)受體拮抗劑(MK-801液)對創傷後大鼠腦線粒體呼吸功能的影響,併探討可能的作用機製,為臨床應用MK-801治療創傷性顱腦損傷提供依據。方法將Wistar大鼠80隻隨機分為4組:對照組20隻,創傷未治組(非治療組)20隻,治療24h組(治療Ⅰ組)20隻,治療72h組(治療Ⅱ組)20隻。採用BIM-Ⅲ型小型多功能生物撞擊機造成大鼠中型顱腦損傷,用氧電極法分析線粒體呼吸功能(呼吸Ⅲ、Ⅳ態和呼吸控製率),併行透視電鏡觀察線粒體超微結構。結果(1)與對照組比較,非治療組傷後72h呼吸Ⅲ態和呼吸控製率明顯下降;治療Ⅰ組呼吸功能有所恢複;治療Ⅱ組呼吸Ⅲ態和呼吸控製率較治療療Ⅰ組有顯著升高(P<0.05),呼吸Ⅳ態稍有延長,但相差不顯著。(2)與對照組比較,電鏡結果示傷後非治療組與治療Ⅰ組、Ⅱ組線粒體結構均有不同程度的損害,但治療Ⅰ組、Ⅱ組線粒體損害程度減輕。結論創傷性顱腦損傷後腦線粒體呼吸功能明顯下降。應用MK-801治療顱腦損傷大鼠可明顯改善腦線粒體呼吸功能,電鏡觀察也髮現線粒體超微結構損害程度減輕。治療時間越長,呼吸功能改善越明顯。
목적관찰N-갑기-D-천문동안산(N-mechy1 D-aspartate,NMDA)수체길항제(MK-801액)대창상후대서뇌선립체호흡공능적영향,병탐토가능적작용궤제,위림상응용MK-801치료창상성로뇌손상제공의거。방법장Wistar대서80지수궤분위4조:대조조20지,창상미치조(비치료조)20지,치료24h조(치료Ⅰ조)20지,치료72h조(치료Ⅱ조)20지。채용BIM-Ⅲ형소형다공능생물당격궤조성대서중형로뇌손상,용양전겁법분석선립체호흡공능(호흡Ⅲ、Ⅳ태화호흡공제솔),병행투시전경관찰선립체초미결구。결과(1)여대조조비교,비치료조상후72h호흡Ⅲ태화호흡공제솔명현하강;치료Ⅰ조호흡공능유소회복;치료Ⅱ조호흡Ⅲ태화호흡공제솔교치료료Ⅰ조유현저승고(P<0.05),호흡Ⅳ태초유연장,단상차불현저。(2)여대조조비교,전경결과시상후비치료조여치료Ⅰ조、Ⅱ조선립체결구균유불동정도적손해,단치료Ⅰ조、Ⅱ조선립체손해정도감경。결론창상성로뇌손상후뇌선립체호흡공능명현하강。응용MK-801치료로뇌손상대서가명현개선뇌선립체호흡공능,전경관찰야발현선립체초미결구손해정도감경。치료시간월장,호흡공능개선월명현。
Objective To study the effects of MK-801 on brain mitochondrial respiratory function in rats after experimental traumatic brain injury and the possible mechanisms .Methods A total of 80 Wistar rats were randomly divided into 4 groups:control group with 20 rats, untreated group ( non-traumatic therapy group ) with 20 rats,24 hours treatment group (treatment group 1) with 20 rats,72 hours treatment group (treatment group 2) with 20 rats.The middle degree brain injury in rats was made by BIM-Ⅲmulti-function impacting machine .The brain cell mitochondrial respiratory function was measured with oxygen electrode and the ultrastructure changes were ob -served with transmission electron microscope .Results (1) Compared with the control group ,the brain mitochon-drial respiratory function reduced significantly in the untreated group within 72 hours.Treatment group 1 showed certain degrees of attenuation ,and treatment group 2 showed further improvement .(2) Compared with the control group,the ultrastructural characteristics in the control group remained nomal ,while the other three groups(untreated group,treatment group l and treatment group 2) had different degrees of mitochondrial ultrastructural damage ,which could be attenuated after the treatment of magnesium sulfate .Conclusion The mitochondrial respiratory function decreased significantly after traumatic brain injury .MK-801 could improve the mitochondrial respiratory function in rats after traumatic injury.It could also attenuate the mitochondrial ultrastructural damage .The curative effectis correlated with the course of treatment .The longer the course of treatment ,the better the improvement of mitochon-drial respiratory function .