中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2011年
5期
630-633
,共4页
唐莹%刘金东%李新巧%薛红%许鹏程
唐瑩%劉金東%李新巧%薛紅%許鵬程
당형%류금동%리신교%설홍%허붕정
1-磷脂酰肌醇3-激酶%蛋白质丝氨酸苏氨酸激酶%麻醉药%吸入%缺血预处理%心肌再灌注损伤
1-燐脂酰肌醇3-激酶%蛋白質絲氨痠囌氨痠激酶%痳醉藥%吸入%缺血預處理%心肌再灌註損傷
1-린지선기순3-격매%단백질사안산소안산격매%마취약%흡입%결혈예처리%심기재관주손상
1-phosphatidylinositol 3-kinase%Protein-serine-threonine kinases%Anesthetics,inhalation%Ischemic preconditioning%Myocardial reperfusion injury
目的 评价磷脂酰肌醇-3-激酶-丝氨酸/苏氨酸激酶(PI3K-Akt)信号通路在七氟醚预处理减轻大鼠离体心脏缺血再灌注损伤中的作用.方法 健康成年雄性SD大鼠96只,体重220～280g,采用随机数字表法,将其随机分为6组(n=16):假手术组(S组)、缺血再灌注组(I/R组)、七氟醚预处理组(SP组)、渥曼青霉素组(W组)、二甲基亚砜组(D组)和七氟醚预处理+渥曼青霉素组(SW组).采用Langendorff装置建立大鼠离体心脏缺血再灌注模型.S组继续灌注180 min;I/R组平衡灌注30 min,缺血30 min,恢复灌注120 min;其余各组先平衡灌注15 min,SP组、W组、DMSO组和SW组分别用含2.4%七氟醚、100 nmol/L渥曼青霉察、20 μmol/L二甲基亚砜、2.4%七氟醚和100 nmol/L渥曼青霉素的K-H液灌注10 min,然后洗脱5 min,缺血30 min,恢复灌注120 min.各组随机取8个心脏,于平衡灌注末和再灌注15 min时,记录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15 min时取心肌组织,采用TUNEL法检测细胞凋亡,计算凋亡指数;采用Western blot法测定磷酸化Akt(p-Akt)表达.再灌注120 min时,取8个心脏,采用TIC染色法测定心肌梗死体积.结果 与S组比较,其余各组HR、LVDP和±dp/dtmax降低,LVEDP升高,I/R组、SP组和D组心肌p-Akt表达上调(P＜0.05);与I/R组比较,SP组LVDP和±dp/dtmax升高,LVEDP和凋亡指数降低,心肌p-Akt表达上调,心肌梗死体积减小(P＜0.05),SW组上述指标差异无统计学意义(P＞0.05).结论 七氟醚预处理可通过激活PI3K-Akt信号通路减轻大鼠离体心脏缺血再灌注损伤.
目的 評價燐脂酰肌醇-3-激酶-絲氨痠/囌氨痠激酶(PI3K-Akt)信號通路在七氟醚預處理減輕大鼠離體心髒缺血再灌註損傷中的作用.方法 健康成年雄性SD大鼠96隻,體重220～280g,採用隨機數字錶法,將其隨機分為6組(n=16):假手術組(S組)、缺血再灌註組(I/R組)、七氟醚預處理組(SP組)、渥曼青黴素組(W組)、二甲基亞砜組(D組)和七氟醚預處理+渥曼青黴素組(SW組).採用Langendorff裝置建立大鼠離體心髒缺血再灌註模型.S組繼續灌註180 min;I/R組平衡灌註30 min,缺血30 min,恢複灌註120 min;其餘各組先平衡灌註15 min,SP組、W組、DMSO組和SW組分彆用含2.4%七氟醚、100 nmol/L渥曼青黴察、20 μmol/L二甲基亞砜、2.4%七氟醚和100 nmol/L渥曼青黴素的K-H液灌註10 min,然後洗脫5 min,缺血30 min,恢複灌註120 min.各組隨機取8箇心髒,于平衡灌註末和再灌註15 min時,記錄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15 min時取心肌組織,採用TUNEL法檢測細胞凋亡,計算凋亡指數;採用Western blot法測定燐痠化Akt(p-Akt)錶達.再灌註120 min時,取8箇心髒,採用TIC染色法測定心肌梗死體積.結果 與S組比較,其餘各組HR、LVDP和±dp/dtmax降低,LVEDP升高,I/R組、SP組和D組心肌p-Akt錶達上調(P＜0.05);與I/R組比較,SP組LVDP和±dp/dtmax升高,LVEDP和凋亡指數降低,心肌p-Akt錶達上調,心肌梗死體積減小(P＜0.05),SW組上述指標差異無統計學意義(P＞0.05).結論 七氟醚預處理可通過激活PI3K-Akt信號通路減輕大鼠離體心髒缺血再灌註損傷.
목적 평개린지선기순-3-격매-사안산/소안산격매(PI3K-Akt)신호통로재칠불미예처리감경대서리체심장결혈재관주손상중적작용.방법 건강성년웅성SD대서96지,체중220～280g,채용수궤수자표법,장기수궤분위6조(n=16):가수술조(S조)、결혈재관주조(I/R조)、칠불미예처리조(SP조)、악만청매소조(W조)、이갑기아풍조(D조)화칠불미예처리+악만청매소조(SW조).채용Langendorff장치건립대서리체심장결혈재관주모형.S조계속관주180 min;I/R조평형관주30 min,결혈30 min,회복관주120 min;기여각조선평형관주15 min,SP조、W조、DMSO조화SW조분별용함2.4%칠불미、100 nmol/L악만청매찰、20 μmol/L이갑기아풍、2.4%칠불미화100 nmol/L악만청매소적K-H액관주10 min,연후세탈5 min,결혈30 min,회복관주120 min.각조수궤취8개심장,우평형관주말화재관주15 min시,기록HR、좌실서장말압(LVEDP)、좌실발전압(LVDP)、좌심실내압최대상승속솔(+dp/dtmax)화좌심실내압최대하강속솔(-dp/dtmax).재관주15 min시취심기조직,채용TUNEL법검측세포조망,계산조망지수;채용Western blot법측정린산화Akt(p-Akt)표체.재관주120 min시,취8개심장,채용TIC염색법측정심기경사체적.결과 여S조비교,기여각조HR、LVDP화±dp/dtmax강저,LVEDP승고,I/R조、SP조화D조심기p-Akt표체상조(P＜0.05);여I/R조비교,SP조LVDP화±dp/dtmax승고,LVEDP화조망지수강저,심기p-Akt표체상조,심기경사체적감소(P＜0.05),SW조상술지표차이무통계학의의(P＞0.05).결론 칠불미예처리가통과격활PI3K-Akt신호통로감경대서리체심장결혈재관주손상.
Objective To investigate the role of phosphatidyl-inositol 3-kinase-Akt (PI3k-Akt) signal pathway in the attenuation of ischemia-reperfusion (I/R) injury by sevoflurane preconditioning in isolated rat hearts. Methods Ninety-six adult male SD rats weighing 220-280 g were randomly divided into 6 groups ( n = 16 each): sham operation group (group S); I/R group; sevoflurane preconditioning group (group SP); wortmannin group (group W); dimethyl sulfoxide (DMSO) group (group D) and sevoflurane preconditioning + wortmannin group (group SW) . Their hearts were excised and perfused in a Langendorff apparatus with K-H solution saturated with 95%O2-5%C02 at 37 ℃ . The hearts were continuously perfused for 180 min in group S. After 15 min of equilibration, the isolated hearts were subjected to 30 min of ischemia followed by 120 min of reperfusion in SP, W, D and SW groups. Croups SP, W, D and SW received 10 min of perfusion with K-H solution containing 2. 4% sevoflurane, 100 nmol/L wortmannin, 20 μmol/L DMSO, and 2.4% sevoflurane + 100 nmol/L wortmannin, respectively, followed by 5 min washout before I/R. Eight hearts in each group were selected and HR, left ventricular end-diabetic pressure (LVEDP), left ventricular developed pressure (LVDP), and ± dp/dtmax were recorded at the end of equilibration and at 15 min of reperfusion, Myocardial tissues were obtained at 15 min of reperfusion for determination of apoptosis (by TUNEL) and phosphorylated Akt (p-Akt) expression (by Western blot) . Another 8 hearts were selected at 120 min of reperfusion for determination of myocardial infarct size by TTC staining. Result Compared with group S, LVDP and ± dp/dt,^ were significantly decreased and LVEDP was significantly increased in groups I/R, SP, W, D and SW, and myocardial p-Akt expression was up-regulated in groups I/R, SP and D ( P ＜ 0.05). Compared with group I/R, LVDP and ± dp/dtmax were significantly increased, LVEDP and apoptosis index were significantly decreased, myocardial p-Akt expression was up-regulated, and myocardial infarct size was significantly reduced in group SP (P ＜0.05) . Conclusion Activation of PI3K-Akt signal pathway is involved in the attenuation of I/R injury by sevoflurane reconditioning in isolated rat hearts.
