医学研究生学报
醫學研究生學報
의학연구생학보
Journal of Medical Postgraduates
2015年
10期
1028-1033
,共6页
李新灵%张冰%雷钟%杜靖
李新靈%張冰%雷鐘%杜靖
리신령%장빙%뢰종%두정
右美托咪定%肾缺血再灌注%心肌组织%炎症因子
右美託咪定%腎缺血再灌註%心肌組織%炎癥因子
우미탁미정%신결혈재관주%심기조직%염증인자
Dexmedetomidine%Renal ischemia-reperfusion%Myocardial tissue%Inflammatory factor
目的 肾缺血再灌注对心肌组织有损伤,而右美托咪定(Dexmedetomidine, DEX)是一种具有抗交感、镇静和镇痛等作用的新型α2肾上腺素能受体激动剂. 文中旨在探讨DEX对大鼠肾缺血再灌注不同时间心肌组织的影响. 方法 健康成年雄性Wistar大鼠40只,采用随机数字表法将其分为5组( n=8 ):假手术组:仅游离双侧肾蒂,不结扎;肾缺血60 min组、肾缺血120 min组肾切除后,分别结扎左肾动脉60 min、120 min,再灌注3 h;DEX+肾缺血60 min组、DEX+肾缺血120 min组均缺血前30 min腹腔内注射DEX 50μg/kg,分别结扎左肾动脉60 min、120 min,再灌注3 h. 采用右肾切除后左肾缺血再灌注的方法制备肾缺血再灌注损伤模型. 5组均于恢复灌注3 h时经下腔静脉采血5 mL,检测Cr、BUN浓度,并取肾组织和心肌组织,光镜下观察病理学结果,酶联免疫法( ELISA)检测白细胞介素-10 (IL-10 )、肿瘤坏死因子-α( TNF-α)的表达. 结果 ①与假手术组Cr、BUN[(53.20 ±9.21) μmol/L、(3.75 ±0.78) mmol/L]比较,肾缺血60 min组[(84.67 ±9.62) μmol/L、(8.55 ±1.08) mmol/L]、DEX +肾缺血60 min 组[(69.67 ±9.52) μmol/L、(7.56 ±0.70) mmol/L]及肾缺血120 min 组[(167.11 ±18.81) μmol/L、(13.42 ±1.25) mmol/L]、DEX+肾缺血120 min组 [(114.29 ±12.50) μmol/L、(10.27 ±0.78) mmol/L]均升高(P<0.05);假手术组肾组织和心肌组织IL-10、TNF-α浓度较其他4组显著降低(P<0.05),其中DEX+肾缺血60 min组、DEX+肾缺血120 min组分别较对应肾缺血时间组IL-10含量升高,TNF-α含量降低(P<0.05). ②DEX+肾缺血60 min组、DEX+肾缺血120 min组肾组织损伤较其他3组减轻. ③肾缺血60 min组、肾缺血 120 min组大鼠较假手术组心肌组织部分横纹消失,肌浆溶解;DEX+肾缺血60 min组和DEX+肾缺血120 min组较其他3组炎性细胞浸润减少. 结论 右美托咪定可减轻大鼠肾缺血再灌注不同时间引起的远隔器官心肌组织的损伤,其机制可能与抑制炎症因子有关.
目的 腎缺血再灌註對心肌組織有損傷,而右美託咪定(Dexmedetomidine, DEX)是一種具有抗交感、鎮靜和鎮痛等作用的新型α2腎上腺素能受體激動劑. 文中旨在探討DEX對大鼠腎缺血再灌註不同時間心肌組織的影響. 方法 健康成年雄性Wistar大鼠40隻,採用隨機數字錶法將其分為5組( n=8 ):假手術組:僅遊離雙側腎蒂,不結扎;腎缺血60 min組、腎缺血120 min組腎切除後,分彆結扎左腎動脈60 min、120 min,再灌註3 h;DEX+腎缺血60 min組、DEX+腎缺血120 min組均缺血前30 min腹腔內註射DEX 50μg/kg,分彆結扎左腎動脈60 min、120 min,再灌註3 h. 採用右腎切除後左腎缺血再灌註的方法製備腎缺血再灌註損傷模型. 5組均于恢複灌註3 h時經下腔靜脈採血5 mL,檢測Cr、BUN濃度,併取腎組織和心肌組織,光鏡下觀察病理學結果,酶聯免疫法( ELISA)檢測白細胞介素-10 (IL-10 )、腫瘤壞死因子-α( TNF-α)的錶達. 結果 ①與假手術組Cr、BUN[(53.20 ±9.21) μmol/L、(3.75 ±0.78) mmol/L]比較,腎缺血60 min組[(84.67 ±9.62) μmol/L、(8.55 ±1.08) mmol/L]、DEX +腎缺血60 min 組[(69.67 ±9.52) μmol/L、(7.56 ±0.70) mmol/L]及腎缺血120 min 組[(167.11 ±18.81) μmol/L、(13.42 ±1.25) mmol/L]、DEX+腎缺血120 min組 [(114.29 ±12.50) μmol/L、(10.27 ±0.78) mmol/L]均升高(P<0.05);假手術組腎組織和心肌組織IL-10、TNF-α濃度較其他4組顯著降低(P<0.05),其中DEX+腎缺血60 min組、DEX+腎缺血120 min組分彆較對應腎缺血時間組IL-10含量升高,TNF-α含量降低(P<0.05). ②DEX+腎缺血60 min組、DEX+腎缺血120 min組腎組織損傷較其他3組減輕. ③腎缺血60 min組、腎缺血 120 min組大鼠較假手術組心肌組織部分橫紋消失,肌漿溶解;DEX+腎缺血60 min組和DEX+腎缺血120 min組較其他3組炎性細胞浸潤減少. 結論 右美託咪定可減輕大鼠腎缺血再灌註不同時間引起的遠隔器官心肌組織的損傷,其機製可能與抑製炎癥因子有關.
목적 신결혈재관주대심기조직유손상,이우미탁미정(Dexmedetomidine, DEX)시일충구유항교감、진정화진통등작용적신형α2신상선소능수체격동제. 문중지재탐토DEX대대서신결혈재관주불동시간심기조직적영향. 방법 건강성년웅성Wistar대서40지,채용수궤수자표법장기분위5조( n=8 ):가수술조:부유리쌍측신체,불결찰;신결혈60 min조、신결혈120 min조신절제후,분별결찰좌신동맥60 min、120 min,재관주3 h;DEX+신결혈60 min조、DEX+신결혈120 min조균결혈전30 min복강내주사DEX 50μg/kg,분별결찰좌신동맥60 min、120 min,재관주3 h. 채용우신절제후좌신결혈재관주적방법제비신결혈재관주손상모형. 5조균우회복관주3 h시경하강정맥채혈5 mL,검측Cr、BUN농도,병취신조직화심기조직,광경하관찰병이학결과,매련면역법( ELISA)검측백세포개소-10 (IL-10 )、종류배사인자-α( TNF-α)적표체. 결과 ①여가수술조Cr、BUN[(53.20 ±9.21) μmol/L、(3.75 ±0.78) mmol/L]비교,신결혈60 min조[(84.67 ±9.62) μmol/L、(8.55 ±1.08) mmol/L]、DEX +신결혈60 min 조[(69.67 ±9.52) μmol/L、(7.56 ±0.70) mmol/L]급신결혈120 min 조[(167.11 ±18.81) μmol/L、(13.42 ±1.25) mmol/L]、DEX+신결혈120 min조 [(114.29 ±12.50) μmol/L、(10.27 ±0.78) mmol/L]균승고(P<0.05);가수술조신조직화심기조직IL-10、TNF-α농도교기타4조현저강저(P<0.05),기중DEX+신결혈60 min조、DEX+신결혈120 min조분별교대응신결혈시간조IL-10함량승고,TNF-α함량강저(P<0.05). ②DEX+신결혈60 min조、DEX+신결혈120 min조신조직손상교기타3조감경. ③신결혈60 min조、신결혈 120 min조대서교가수술조심기조직부분횡문소실,기장용해;DEX+신결혈60 min조화DEX+신결혈120 min조교기타3조염성세포침윤감소. 결론 우미탁미정가감경대서신결혈재관주불동시간인기적원격기관심기조직적손상,기궤제가능여억제염증인자유관.
Objectiv e Renal ischemia-reperfusion ( I/R) may cause myocardial injury and dexmedetomidine ( DEX) is a new alpha-2 adrenergic agonist with the effects of antisympathia , seda-tion, and analgesia.This study was to investigate the effect of DEX on the myocardial tissue of rats at different time points after renal I/R. Methods Forty male Wistar rats were randomized into 5 groups of equal number,sham operation, 60 min renal ischemia and 3 h reperfusion (I/R1), 120 min ischemia and 3 h reperfusion (I/R2 ), 60 min ischemia and DEX+3 h reperfusion (D1), 120 min ischemia and DEX+3 h reperfusion ( D2) .Renal I/R was induced by removal of the right kidney and ligation of the left re-nal artery and vein followed by 3 hours of reperfusion.Meanwhile, intraperitoneal injection of DEX at 50μg/kg was given to the ani-mals in groups D1 and D2 at 60 at 120 min respectively after ischemia.After 3 hours of reperfusion, blood samples were collected for measurement of the concentrations of serum creatinine (Cr) and blood urea nitrogen (BUN), and renal and myocardial tissues harvested for observation of pathological changes under the light microscope and determination of the expressions of TNF-αand IL-10 by ELISA.Results Significant increases were observed in the concentrations of serum Cr and BUN , the expressions of TNF-αand IL-10 in the renal tissues and those in the myocardial tissues in groups I /R1([84.67 ±9.62] μmol/L, [8.55 ±1.08] mmol /L), I/R2 ([167.11 ±18.81] μmol/L, [13.42 ±1.25] mmol/L), D1 ([69.67 ±9.52] μmol/L, [7.56 ±0.70] mmol/L), and D2 ([114.29 ±12.50] μmol/L, [10.27 ±0.78] mmol/L), as compared with the sham operation group ([53.20 ±9.21] μmol/L, [3.75 ±0.78] mmol/L), (all P <0.05).Significant decreases was observed in the sham operation group as compared with other groups in the expressions of TNF-αand IL-10 (P<0.05).Significant decreases was observed in the D1 and D2 groups compared with other groups in the expressions of TNF-α, but increasing in IL-10.②Injury was reduced in the D1 and D2 groups compared with other groups.③The horizontal stripes of myocardial tissue disappeared in I/R1 and I/R2 decreases of inflammatory cells was observed in D1 and D2 groups compared with others. Conclusion Dexmedetomidine can attenuate myocar-dial injury induced by renal ischemia-reperfusion in rats and its inhibitory effect on inflammatory factors may be involved in the mechanism.
