中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2014年
10期
1263-1266
,共4页
田环环%邓倩%庞韵婷%邓甘林%刘金东
田環環%鄧倩%龐韻婷%鄧甘林%劉金東
전배배%산천%방운정%산감림%류금동
麻醉药,吸入%缺血预处理%心肌再灌注损伤%紧密连接部
痳醉藥,吸入%缺血預處理%心肌再灌註損傷%緊密連接部
마취약,흡입%결혈예처리%심기재관주손상%긴밀련접부
Anesthetics,inhalation%Ischemic preconditioning%Myocardial reperfusion injury%Tight junctions
目的 评价七氟醚预处理对大鼠心肌缺血再灌注时紧密连接蛋白1(ZO-1)的影响.方法 成年雄性Wistar大鼠,体重250 ～ 300 g,建立Langendorff离体心脏灌注模型.取离体心脏模型18个,采用随机数字表法,将其分成3组(n=6):对照组(C组)、缺血再灌注组(I/R组)和七氟醚预处理组(S组).平衡灌注10 min后,C组继续灌注K-H液110 min;I/R组继续灌注K-H液20 min,全心缺血30 min,再灌注60min;S组灌注经3％七氟醚预充饱和的K-H液15 min,洗脱5 min,全心缺血30 min,再灌注60 min.分别于平衡灌注末、缺血前即刻、再灌注15和60 min时记录心率(HR)、左室舒张末压(LVEDP)、左室发展压(LVDP)、左心室内压最大上升速率(+dp/dtmax)和左心室内压最大下降速率(-dp/dtmax).再灌注期间记录心律失常的发生情况,并进行评分.于再灌注60 min时取心尖部组织,采用Western blot法检测ZO-1表达;免疫荧光法测定ZO-1和缝隙连接蛋白43(Cx43)的分布情况.结果 与C组比较,I/R组再灌注15和60 min时HR、LVDP、+dp/dtmax和-dp/dtmax降低,LVEDP和心律失常评分升高,心肌组织ZO-1表达下调,ZO-1再分布率升高(P＜0.05).与I/R组比较,S组再灌注15和60 min时HR、LVDP、+dp/dtmax和-dp/dtmax升高,LVEDP和心律失常评分降低,心肌组织ZO-1表达上调(P＜0.05).C组ZO-1与Cx43共定位于闰盘处;I/R组位于闰盘处的ZO-1再分布至心肌细胞侧膜,并在侧膜与Cx43发生共定位;S组ZO-1再分布率降低(P＜0.05).结论 七氟醚预处理降低大鼠再灌注性心律失常发生的机制与抑制ZO-1的表达下调和再分布,从而抑制Cx43的再分布有关.
目的 評價七氟醚預處理對大鼠心肌缺血再灌註時緊密連接蛋白1(ZO-1)的影響.方法 成年雄性Wistar大鼠,體重250 ～ 300 g,建立Langendorff離體心髒灌註模型.取離體心髒模型18箇,採用隨機數字錶法,將其分成3組(n=6):對照組(C組)、缺血再灌註組(I/R組)和七氟醚預處理組(S組).平衡灌註10 min後,C組繼續灌註K-H液110 min;I/R組繼續灌註K-H液20 min,全心缺血30 min,再灌註60min;S組灌註經3％七氟醚預充飽和的K-H液15 min,洗脫5 min,全心缺血30 min,再灌註60 min.分彆于平衡灌註末、缺血前即刻、再灌註15和60 min時記錄心率(HR)、左室舒張末壓(LVEDP)、左室髮展壓(LVDP)、左心室內壓最大上升速率(+dp/dtmax)和左心室內壓最大下降速率(-dp/dtmax).再灌註期間記錄心律失常的髮生情況,併進行評分.于再灌註60 min時取心尖部組織,採用Western blot法檢測ZO-1錶達;免疫熒光法測定ZO-1和縫隙連接蛋白43(Cx43)的分佈情況.結果 與C組比較,I/R組再灌註15和60 min時HR、LVDP、+dp/dtmax和-dp/dtmax降低,LVEDP和心律失常評分升高,心肌組織ZO-1錶達下調,ZO-1再分佈率升高(P＜0.05).與I/R組比較,S組再灌註15和60 min時HR、LVDP、+dp/dtmax和-dp/dtmax升高,LVEDP和心律失常評分降低,心肌組織ZO-1錶達上調(P＜0.05).C組ZO-1與Cx43共定位于閏盤處;I/R組位于閏盤處的ZO-1再分佈至心肌細胞側膜,併在側膜與Cx43髮生共定位;S組ZO-1再分佈率降低(P＜0.05).結論 七氟醚預處理降低大鼠再灌註性心律失常髮生的機製與抑製ZO-1的錶達下調和再分佈,從而抑製Cx43的再分佈有關.
목적 평개칠불미예처리대대서심기결혈재관주시긴밀련접단백1(ZO-1)적영향.방법 성년웅성Wistar대서,체중250 ～ 300 g,건립Langendorff리체심장관주모형.취리체심장모형18개,채용수궤수자표법,장기분성3조(n=6):대조조(C조)、결혈재관주조(I/R조)화칠불미예처리조(S조).평형관주10 min후,C조계속관주K-H액110 min;I/R조계속관주K-H액20 min,전심결혈30 min,재관주60min;S조관주경3％칠불미예충포화적K-H액15 min,세탈5 min,전심결혈30 min,재관주60 min.분별우평형관주말、결혈전즉각、재관주15화60 min시기록심솔(HR)、좌실서장말압(LVEDP)、좌실발전압(LVDP)、좌심실내압최대상승속솔(+dp/dtmax)화좌심실내압최대하강속솔(-dp/dtmax).재관주기간기록심률실상적발생정황,병진행평분.우재관주60 min시취심첨부조직,채용Western blot법검측ZO-1표체;면역형광법측정ZO-1화봉극련접단백43(Cx43)적분포정황.결과 여C조비교,I/R조재관주15화60 min시HR、LVDP、+dp/dtmax화-dp/dtmax강저,LVEDP화심률실상평분승고,심기조직ZO-1표체하조,ZO-1재분포솔승고(P＜0.05).여I/R조비교,S조재관주15화60 min시HR、LVDP、+dp/dtmax화-dp/dtmax승고,LVEDP화심률실상평분강저,심기조직ZO-1표체상조(P＜0.05).C조ZO-1여Cx43공정위우윤반처;I/R조위우윤반처적ZO-1재분포지심기세포측막,병재측막여Cx43발생공정위;S조ZO-1재분포솔강저(P＜0.05).결론 칠불미예처리강저대서재관주성심률실상발생적궤제여억제ZO-1적표체하조화재분포,종이억제Cx43적재분포유관.
Objective To evaluate the effects of sevoflurane preconditioning on zonula occludens-1 (ZO-1) during myocardial ischemia-reperfusion (I/R) in rats in vitro.Methods Adult male Wistar rats,weighing 250-300 g,were anesthetized with intraperitoneal pentobarbital 30 mg/kg and heparinized.Their hearts were excised and perfused in a Langendorff apparatus with K-H solution saturated with 95％ O2-5％ CO2 at 37 ℃.Eighteen isolated rat hearts were randomly assigned into 3 groups (n =6 each) using a random number table:control group (group C),group I/R and sevoflurane preconditioning group (group S).At 10 min of equilibration,the hearts were perfused with K-H solution for 110 min in group C,the hearts were perfused with K-H solution for 20 min,and then subjected to 30 min of ischemia followed by 60 min of reperfusion in group I/R,and the hearts were perfused with K-H solution saturated with 3％ sevoflurane for 15 min followed by 5 min washout,and then subjected to 30 min of ischemia followed by 60 min of reperfusion in group S.At the end of equilibration,immediately before ischemia,and at 15 and 60 min of reperfusion (T1,2),HR,left ventricular end-diastolic pressure (LVEDP),left ventricular developed pressure (LVDP),+ dp/dtmax and-dp/dtmax were recorded.The development of arrhythmias was recorded during reperfusion and scored.At 60 min of reperfusion,myocardial specimens were obtained from the apex of heart for determination of the expression of ZO-1 in myocardial tissues (by Western blot) and for observation of distribution of ZO-1 and connexin43 (Cx43) (by immunofluorescence).Results Compared with group C,HR,LVDP,+ dp/dtmax and-dp/dtmax were significantly decreased and LVEDP was increased at 15 and 60 min of reperfusion,scores of arrhythmia was increased,and ZO-1 expression was down-regulated in I/R group.Compared with group I/R,HR,LVDP,+ dp/dtmax and-dp/dtmax were significantly increased and LVEDP was decreased at 15 and 60 min of reperfusion,arrhythmia was decreased,and ZO-1 expression was up-regulated in group S.ZO-1 and Cx43 were co-localized at the intercalated disk.ZO-1 was redistributed in the lateralization of the membrane and co-localized with Cx43 in group I/R.The incidence of ZO-1 lateralization was significantly decreased in group S.Conclusion The mechanism by which sevoflurane preconditioning decreases reperfusion arrhythmia is related to inhibition of down-regulation of expression and redistribution of ZO-1 and inhibition of redistribution of Cx43 in rats.
