当代医学
噹代醫學
당대의학
CHINA CONTEMPORARY MEDICINE
2013年
12期
22-24
,共3页
脑水肿%内皮素%地塞米松
腦水腫%內皮素%地塞米鬆
뇌수종%내피소%지새미송
Cerebral edema%Dexamthasone%Endothelin
目的研究大鼠创伤性脑水肿时内皮素的变化,及地塞米松的治疗作用,并探讨其作用机制.方法采用成年雄性SD大鼠48只,随机分为正常组、假手术组、对照组及治疗组.正常组及假手术组于术后,对照组和治疗组分别在致伤后1 h、6 h、24 h、3 d、7 d处死留取标本,测定脑组织含水量及内皮素含量.结果脑损伤后脑组织含水量与内皮素的变化趋势吻合,且在伤后1 h开始增加,24 h达高峰,持续至3、7 d开始下降;地塞米松治疗组在伤后各时间点脑组织含水量及内皮素含量均较对照组明显下降(P<0.05).结论颅脑损伤后,内皮素可能参与脑水肿的形成和发展,地塞米松可通过抑制内皮素活性,达到改善脑水肿的作用.
目的研究大鼠創傷性腦水腫時內皮素的變化,及地塞米鬆的治療作用,併探討其作用機製.方法採用成年雄性SD大鼠48隻,隨機分為正常組、假手術組、對照組及治療組.正常組及假手術組于術後,對照組和治療組分彆在緻傷後1 h、6 h、24 h、3 d、7 d處死留取標本,測定腦組織含水量及內皮素含量.結果腦損傷後腦組織含水量與內皮素的變化趨勢吻閤,且在傷後1 h開始增加,24 h達高峰,持續至3、7 d開始下降;地塞米鬆治療組在傷後各時間點腦組織含水量及內皮素含量均較對照組明顯下降(P<0.05).結論顱腦損傷後,內皮素可能參與腦水腫的形成和髮展,地塞米鬆可通過抑製內皮素活性,達到改善腦水腫的作用.
목적연구대서창상성뇌수종시내피소적변화,급지새미송적치료작용,병탐토기작용궤제.방법채용성년웅성SD대서48지,수궤분위정상조、가수술조、대조조급치료조.정상조급가수술조우술후,대조조화치료조분별재치상후1 h、6 h、24 h、3 d、7 d처사류취표본,측정뇌조직함수량급내피소함량.결과뇌손상후뇌조직함수량여내피소적변화추세문합,차재상후1 h개시증가,24 h체고봉,지속지3、7 d개시하강;지새미송치료조재상후각시간점뇌조직함수량급내피소함량균교대조조명현하강(P<0.05).결론로뇌손상후,내피소가능삼여뇌수종적형성화발전,지새미송가통과억제내피소활성,체도개선뇌수종적작용.
@@@@Objective To observe the effect of dexamthasone on endothelin level after brain trauma of rats, and to discuss the mechanism of dexamthasone. Methods Forty-eight rats were divided to three groups randomLy:normal group, sham-operated group, control group and treatment group. The level of ET were measured at different points of time after hitting:normal group and sham-group in postoperative, control group and treatment group in different points of time after hitting (1 h,6 h,24 h,3 d,7 d). Results The change tendency of brain water content and endothelin is in coincide, and at 1 hour start to increase, reached its peak at 24 th h, lasted to 3 rd day, and then began to reduce at 7 th day. The treatment group of dexamthasone at different points of time’s water content and endothelin were inferior to the control group, and the difference was statistically significant(P<0.05). Conclusion After brian trauma, dexamthasone appears to be associated with the development of cerebral edema. Dexamthasone improve cerebral edema by inhibiting the activity of endothelin