中国医学创新
中國醫學創新
중국의학창신
MEDICAL INNOVATION OF CHINA
2013年
32期
8-10
,共3页
右美托咪定%缺血预处理%再灌注损伤%肝
右美託咪定%缺血預處理%再灌註損傷%肝
우미탁미정%결혈예처리%재관주손상%간
Dexmedetomidine%Preconditioning%Reperfusion injury%Live
目的：通过右美托咪定预处理对大鼠缺血再灌注肝脏TNF-α及ICAM-1表达的影响，探讨其对肝脏缺血再灌注的保护作用。方法：SD成年雄性大鼠30只，体重150~220 g。随机平均分为3组，每组10只，分别为假手术组（S组），缺血再灌注组（IR组），右美托咪定组（Dex组）。S组和IR组用1 mL/（kg·h）速度静脉滴注0.9%生理盐水30 min；Dex组用右美托咪定5μg/（kg·h）预处理30 min。间隔2 h后IR组和Dex组建立肝脏缺血再灌注模型，S组开腹后不作缺血再灌注。缺血1 h后行再灌注4 h，然后处死大鼠取材。测定大鼠血清ALT和AST，检测肝组织TNF-α活性和ICAM-1水平，观察大鼠组织学病理改变。结果：与S组比较，IR组和Dex组血清ALT、AST和肝组织TNF-α和ICAM-1表达明显升高。Dex组血清ALT、AST酶升高幅度明显较IR组小，肝组织TNF-α和ICAM-1表达低于IR组，肝细胞损伤程度小于缺血再灌注组。结论：右美托咪定预处理能抑制肝缺血再灌注细胞的TNF-α和ICAM-1表达；TNF-α可能通过调控ICAM-1的表达在缺血再灌注损伤中发挥作用。
目的：通過右美託咪定預處理對大鼠缺血再灌註肝髒TNF-α及ICAM-1錶達的影響，探討其對肝髒缺血再灌註的保護作用。方法：SD成年雄性大鼠30隻，體重150~220 g。隨機平均分為3組，每組10隻，分彆為假手術組（S組），缺血再灌註組（IR組），右美託咪定組（Dex組）。S組和IR組用1 mL/（kg·h）速度靜脈滴註0.9%生理鹽水30 min；Dex組用右美託咪定5μg/（kg·h）預處理30 min。間隔2 h後IR組和Dex組建立肝髒缺血再灌註模型，S組開腹後不作缺血再灌註。缺血1 h後行再灌註4 h，然後處死大鼠取材。測定大鼠血清ALT和AST，檢測肝組織TNF-α活性和ICAM-1水平，觀察大鼠組織學病理改變。結果：與S組比較，IR組和Dex組血清ALT、AST和肝組織TNF-α和ICAM-1錶達明顯升高。Dex組血清ALT、AST酶升高幅度明顯較IR組小，肝組織TNF-α和ICAM-1錶達低于IR組，肝細胞損傷程度小于缺血再灌註組。結論：右美託咪定預處理能抑製肝缺血再灌註細胞的TNF-α和ICAM-1錶達；TNF-α可能通過調控ICAM-1的錶達在缺血再灌註損傷中髮揮作用。
목적：통과우미탁미정예처리대대서결혈재관주간장TNF-α급ICAM-1표체적영향，탐토기대간장결혈재관주적보호작용。방법：SD성년웅성대서30지，체중150~220 g。수궤평균분위3조，매조10지，분별위가수술조（S조），결혈재관주조（IR조），우미탁미정조（Dex조）。S조화IR조용1 mL/（kg·h）속도정맥적주0.9%생리염수30 min；Dex조용우미탁미정5μg/（kg·h）예처리30 min。간격2 h후IR조화Dex조건립간장결혈재관주모형，S조개복후불작결혈재관주。결혈1 h후행재관주4 h，연후처사대서취재。측정대서혈청ALT화AST，검측간조직TNF-α활성화ICAM-1수평，관찰대서조직학병리개변。결과：여S조비교，IR조화Dex조혈청ALT、AST화간조직TNF-α화ICAM-1표체명현승고。Dex조혈청ALT、AST매승고폭도명현교IR조소，간조직TNF-α화ICAM-1표체저우IR조，간세포손상정도소우결혈재관주조。결론：우미탁미정예처리능억제간결혈재관주세포적TNF-α화ICAM-1표체；TNF-α가능통과조공ICAM-1적표체재결혈재관주손상중발휘작용。
Objective: To observe the effect of dexmedetomidine preconditioning on hepatic ischemia-reperfusion injury in rats and investigate the role of TNF-α and ICAM-1 in hepatic ischemia-reperfusion injury. Method: Thirty adult male SD rats of weighing 150-220 g were randomly divided into 3 groups of sham-operated group(S group), ischemia-reperfusion group(IR group) and dexmedetomidine group(Dex group),each group of 10 cases. S group and IR group were injected 0.9% saline 1 mL/(kg·h) for 30 min. Dex group were injected dexmedetomidine 5μg/(kg·h) for 30 min. IR group and Dex group animals were administrated hepatic ischemic 1 hours after 2 hours. Then reperfusion was done 4 hours after hepatic ischemia. The animals were killed after reperfusion. Then the specimens of liver tissues and blood were obtained. Serum ALT, AST and the levels of TNF-α and ICAM-1 in the hepatic tissues were detected. The liver tissues were observed with microscopic examination. Result: Compared with S group, ALT, AST and the expression of TNF-α and ICAM-1 were significantly higher in Dex group and IR group. In Dex group, ALT and AST were significantly lower than IR group. The expression of TNF-α and ICAM-1 in Dex group were also significantly lower. Microscopy examination showed the degree of injury in Dex group was smaller than that in IR group. Conclusion: The expression of TNF-α and ICAM-1 could be inhibited by dexmedetomidine preconditioning before hepatic ischemia-reperfusion. The expression of ICAM-1 may be regulated by TNF-α in ischemia-reperfusion injury.
