中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2014年
4期
477-480
,共4页
张静%乔世刚%胡素梅%殷明%曹建方%王琛
張靜%喬世剛%鬍素梅%慇明%曹建方%王琛
장정%교세강%호소매%은명%조건방%왕침
麻醉药,吸入%心肌再灌注损伤%细胞凋亡%核糖体蛋白质S6激酶类,70-kDa
痳醉藥,吸入%心肌再灌註損傷%細胞凋亡%覈糖體蛋白質S6激酶類,70-kDa
마취약,흡입%심기재관주손상%세포조망%핵당체단백질S6격매류,70-kDa
Anesthetics,inhalation%Myocardial reperfusion injury%Apoptosis%Ribosomal protein S6 kinases,70-kDa
目的 评价七氟醚后处理对大鼠离体心脏缺血再灌注时心肌细胞核糖体40S小亚基蛋白S6激酶(p70S6K)表达的影响.方法 取Langendorff心脏模型制备成功的大鼠心脏90个,采用随机数字表法分为3组(n=30):假手术组(S组)、缺血再灌注组(I/R组)和七氟醚后处理组(SP组).离体心脏缺血30 min,再灌注2h.SP组于缺血末至再灌注15 min灌注经3.0%七氟醚饱和的K-H液,随后更换为正常K-H液再灌注105 min.于再灌注2h时测定心肌梗死体积,计算心肌梗死体积百分比,采用Western blot法检测心肌细胞p-p70S6K/t-p70S6K、细胞质和线粒体细胞色素c和caspase-8的表达水平.结果 与S组比较,I/R组心肌梗死体积百分比升高,心肌细胞p-p70S6K/t-p70S6K、细胞质细胞色素c和caspase-8表达上调,线粒体细胞色素c表达下调(P<0.05);与I/R组比较,SP组心肌梗死体积百分比降低,心肌细胞p-p70S6K/t-p70S6K和线粒体细胞色素c表达上调,细胞质细胞色素c和caspase-8表达下调(P<0.05).结论 七氟醚后处理可减轻离体大鼠离体心脏缺血再灌注损伤,其机制与上调心肌细胞p-p70S6K表达,抑制线粒体细胞色素c转移至细胞质,从而减少细胞凋亡有关.
目的 評價七氟醚後處理對大鼠離體心髒缺血再灌註時心肌細胞覈糖體40S小亞基蛋白S6激酶(p70S6K)錶達的影響.方法 取Langendorff心髒模型製備成功的大鼠心髒90箇,採用隨機數字錶法分為3組(n=30):假手術組(S組)、缺血再灌註組(I/R組)和七氟醚後處理組(SP組).離體心髒缺血30 min,再灌註2h.SP組于缺血末至再灌註15 min灌註經3.0%七氟醚飽和的K-H液,隨後更換為正常K-H液再灌註105 min.于再灌註2h時測定心肌梗死體積,計算心肌梗死體積百分比,採用Western blot法檢測心肌細胞p-p70S6K/t-p70S6K、細胞質和線粒體細胞色素c和caspase-8的錶達水平.結果 與S組比較,I/R組心肌梗死體積百分比升高,心肌細胞p-p70S6K/t-p70S6K、細胞質細胞色素c和caspase-8錶達上調,線粒體細胞色素c錶達下調(P<0.05);與I/R組比較,SP組心肌梗死體積百分比降低,心肌細胞p-p70S6K/t-p70S6K和線粒體細胞色素c錶達上調,細胞質細胞色素c和caspase-8錶達下調(P<0.05).結論 七氟醚後處理可減輕離體大鼠離體心髒缺血再灌註損傷,其機製與上調心肌細胞p-p70S6K錶達,抑製線粒體細胞色素c轉移至細胞質,從而減少細胞凋亡有關.
목적 평개칠불미후처리대대서리체심장결혈재관주시심기세포핵당체40S소아기단백S6격매(p70S6K)표체적영향.방법 취Langendorff심장모형제비성공적대서심장90개,채용수궤수자표법분위3조(n=30):가수술조(S조)、결혈재관주조(I/R조)화칠불미후처리조(SP조).리체심장결혈30 min,재관주2h.SP조우결혈말지재관주15 min관주경3.0%칠불미포화적K-H액,수후경환위정상K-H액재관주105 min.우재관주2h시측정심기경사체적,계산심기경사체적백분비,채용Western blot법검측심기세포p-p70S6K/t-p70S6K、세포질화선립체세포색소c화caspase-8적표체수평.결과 여S조비교,I/R조심기경사체적백분비승고,심기세포p-p70S6K/t-p70S6K、세포질세포색소c화caspase-8표체상조,선립체세포색소c표체하조(P<0.05);여I/R조비교,SP조심기경사체적백분비강저,심기세포p-p70S6K/t-p70S6K화선립체세포색소c표체상조,세포질세포색소c화caspase-8표체하조(P<0.05).결론 칠불미후처리가감경리체대서리체심장결혈재관주손상,기궤제여상조심기세포p-p70S6K표체,억제선립체세포색소c전이지세포질,종이감소세포조망유관.
Objective To evaluate the effects of sevoflurane postconditioning on the expression of 70 kD aribosomalprotein S6 kinase (p70S6K) during ischemia-reperfusion (I/R) in isolated rat hearts.Methods Pathogen-free male Sprague-Dawley rats,aged 3 months,weighing 270-350 g,were used in the study.Their hearts were excised and perfused in a Langendorff apparatus with K-H solution saturated with 95 % O2-5 % CO2.Ninety isolated rat hearts with I/R injury were randomly divided into 3 groups (n =30 each):sham operation group (group S),I/R group (group I/R),and sevoflurane postconditioning group (group SP).The hearts were subjected to ischemia for 30 min followed by 2 h reperfusion.In group SP,the hearts were perfused with K-H solution saturated with 3.0% sevoflurane for 15 min starting from the end of ischemia until 15 min of reperfusion,and then with plain K-H solution for 105 min.At 2 h of reperfusion,myocardial infarct size was measured,the percentage of myocardial infarct size was calculated,and the phosphorylated p70S6K (p-p70S6K)/total p70S6K (tp70S6K) ratio,and cytoplasm,cytochrome C,and caspase-8 expression was measured.Results Compared with group S,the percentage of myocardial infarct size and p-p70S6K/t-p70S6K ratio were significantly increased,the expression of cytochrome C,and caspase-8 was up-regulated,and the expression of cytochrome C was downregulated in I/R group.Compared with I/R group,the percentage of myocardial infarct size was significantly decreased,the ratio of p-p70S6K/t-p70S6K was increased and cytochrome C expression was up-regulated,and the expression of cytochrome C and caspase-8 was down-regulated in SP group.Conclusion Sevoflurane postconditioning can mitigate I/R injury to isolated rat hearts,and up-regulation of p-p70S6K expression,inhibition of transfer of cytochrome C from mitochondria to cytoplasm,and reduced cell apoptosis are involved in the mechanism.