新疆医科大学学报
新疆醫科大學學報
신강의과대학학보
JOURNAL OF XINJIANG MEDICAL UNIVERSITY
2013年
11期
1595-1598,1602
,共5页
陈铀%马依彤%杨毅宁%曹明宇%刘芬%陈邦党%于子翔%李晓梅%贺春晖%沈鑫
陳鈾%馬依彤%楊毅寧%曹明宇%劉芬%陳邦黨%于子翔%李曉梅%賀春暉%瀋鑫
진유%마의동%양의저%조명우%류분%진방당%우자상%리효매%하춘휘%침흠
血糖%缺血后适应%再灌注损伤
血糖%缺血後適應%再灌註損傷
혈당%결혈후괄응%재관주손상
blood glucose%ischemic postconditioning%reperfusion injury
目的：探讨不同血糖水平对离体心脏缺血后适应下血流动力学、心梗面积的差异及其机制。方法12周龄C57/BL雄性小鼠，利用Langendorff灌流装置建立小鼠心肌缺血后适应（IPC）模型。K-H缓冲液临用前配制，方案分正常葡萄糖水平组（NBG组）：11．1mmol/L和高葡萄糖水平组（HBG组）：22．2mmol/L，其他成分两组一致。IPC采用60min全心缺血，再灌注之前给予3次IPC循环，每次10s，再灌注120min。沿左心房置入顶端球囊测压导管进行心脏血流动力学检测；采用三苯基氯化四氮唑染色的方法确定心肌梗死范围；采用Western印迹检测心肌组织RISK信号通路。结果和NBG组比较，HBG组小鼠心脏血流动力学指标左心室收缩压（LVSP）显著下降，差异有统计学意义（P＜0．05），左室舒张末压（LVEDP）差异无统计学意义（P＞0．05），心肌梗死范围增加，差异有统计学意义（P＜0．01）；两组ERK1/2信号通路显著抑制，Akt信号通路表达无明显差异。结论正常水平血糖较高血糖状态下进行缺血后适应处理更能有效地减轻心肌缺血再灌注损伤。
目的：探討不同血糖水平對離體心髒缺血後適應下血流動力學、心梗麵積的差異及其機製。方法12週齡C57/BL雄性小鼠，利用Langendorff灌流裝置建立小鼠心肌缺血後適應（IPC）模型。K-H緩遲液臨用前配製，方案分正常葡萄糖水平組（NBG組）：11．1mmol/L和高葡萄糖水平組（HBG組）：22．2mmol/L，其他成分兩組一緻。IPC採用60min全心缺血，再灌註之前給予3次IPC循環，每次10s，再灌註120min。沿左心房置入頂耑毬囊測壓導管進行心髒血流動力學檢測；採用三苯基氯化四氮唑染色的方法確定心肌梗死範圍；採用Western印跡檢測心肌組織RISK信號通路。結果和NBG組比較，HBG組小鼠心髒血流動力學指標左心室收縮壓（LVSP）顯著下降，差異有統計學意義（P＜0．05），左室舒張末壓（LVEDP）差異無統計學意義（P＞0．05），心肌梗死範圍增加，差異有統計學意義（P＜0．01）；兩組ERK1/2信號通路顯著抑製，Akt信號通路錶達無明顯差異。結論正常水平血糖較高血糖狀態下進行缺血後適應處理更能有效地減輕心肌缺血再灌註損傷。
목적：탐토불동혈당수평대리체심장결혈후괄응하혈류동역학、심경면적적차이급기궤제。방법12주령C57/BL웅성소서，이용Langendorff관류장치건립소서심기결혈후괄응（IPC）모형。K-H완충액림용전배제，방안분정상포도당수평조（NBG조）：11．1mmol/L화고포도당수평조（HBG조）：22．2mmol/L，기타성분량조일치。IPC채용60min전심결혈，재관주지전급여3차IPC순배，매차10s，재관주120min。연좌심방치입정단구낭측압도관진행심장혈류동역학검측；채용삼분기록화사담서염색적방법학정심기경사범위；채용Western인적검측심기조직RISK신호통로。결과화NBG조비교，HBG조소서심장혈류동역학지표좌심실수축압（LVSP）현저하강，차이유통계학의의（P＜0．05），좌실서장말압（LVEDP）차이무통계학의의（P＞0．05），심기경사범위증가，차이유통계학의의（P＜0．01）；량조ERK1/2신호통로현저억제，Akt신호통로표체무명현차이。결론정상수평혈당교고혈당상태하진행결혈후괄응처리경능유효지감경심기결혈재관주손상。
Objective To explore the differences and mechanisms of hemodynamics and myocardial infarct size under different blood glucose levels of ischemic myocardial postconditioning in vitro .Methods Myo-cardial ischemia postconditioning (IPC) models were built with 12-weeks-old C57/BL male mice ,by use of Langendorff perfusion device .K-H buffer was prepared before using .Two groups were divided according to protocal :normal blood glucose (NBG) group with 11 .1 mmol/L ,and high glucose (HBG) group with 22 .2 mmol/L ,other components were the same .The IPC model adopted 60min whole heart ischemia ,3 times IPC cycle were administered before reperfusion ,each time for 10 s ,and reperfusion for 120 min .In-sert top end saccule manometry catheter into the left atriam to detect cardiac hemodynamics .Triphenyl tet-razolium staining method was used to determine the scope of myocardial infarction .Western blot was ap-plied to detect the RISK signaling pathway of myocardial tissue .Results Left ventricular systolic pressure (LVSP) of the cardiac hemodynamic parameters of HBG group mice decreased significantly ,compared with NBG group (P <0 .05);the left ventricular end-diastolic pressure (LVEDP) of two groups had no significant differences (P >0 .05);and the scope of myocardial infarction of HBG group increased ,com-pared with NBG group (P <0 .05) .ERK1/2 signaling pathway was significantly inhibited ,and there was no significant difference of the expression of AKT signaling pathway .Conclusion Compared with the high blood glucose (HBG) group ,the normal blood glucose (NBG) group can be more effectively relieved myo-cardial ischemia-reperfusion injury by ischemic postconditioning treatment .
