中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2013年
3期
357-359
,共3页
李志鹏%李玉娟%何妹仪%何月贞%柳垂亮
李誌鵬%李玉娟%何妹儀%何月貞%柳垂亮
리지붕%리옥연%하매의%하월정%류수량
麻醉药,吸入%再灌注损伤%小肠
痳醉藥,吸入%再灌註損傷%小腸
마취약,흡입%재관주손상%소장
Anesthetics,inhalationg%Reperfusion injury%Intestine,small
目的 评价七氟醚后处理对大鼠肠缺血再灌注损伤的影响.方法 成年雄性SD大鼠36只,体重200 ~ 220 g,采用随机数字表法,将其分为4组(n=9)∶假手术组(Sham组)、肠缺血再灌注组(I/R组)、缺血后处理组(Ipo组)和七氟醚后处理组(Sevo组).I/R组、Ipo组Sevo组采用结扎肠系膜上动脉60 min,再灌注120min的方法制备肠缺血再灌注模型.Ipo组于再灌注即刻恢复血流30 s后再阻断30 s,重复3次行后处理.Sevo组于再灌注即刻吸入1.15%七氟醚30 min行后处理.再灌注120 min时,处死大鼠,取小肠组织,采用Chui评分法行病理学损伤评分;采用TUNEL法计算凋亡细胞密度;采用比色法检测MDA含量和SOD活性;采用Western blot法检测caspase-3蛋白表达.结果 与Sham组相比,I/R组、Sevo组和Ipo组病理学损伤评分、凋亡细胞密度和MDA含量均升高,SOD活性降低,caspase-3蛋白表达上调(P<0.05);与I/R组相比,Sevo组和Ipo组病理学损伤评分、凋亡细胞密度和MDA含量均降低,SOD活性升高,caspase-3蛋白表达下调(P<0.05);Sevo组和Ipo组病理学损伤评分、凋亡细胞密度、MDA含量、SOD活性和caspase-3蛋白表达比较差异无统计学意义(P>0.05).结论 七氟醚后处理可通过减轻脂质过氧化反应和减少细胞凋亡,减轻大鼠肠缺血再灌注损伤,其保护效应与缺血后处理相似.
目的 評價七氟醚後處理對大鼠腸缺血再灌註損傷的影響.方法 成年雄性SD大鼠36隻,體重200 ~ 220 g,採用隨機數字錶法,將其分為4組(n=9)∶假手術組(Sham組)、腸缺血再灌註組(I/R組)、缺血後處理組(Ipo組)和七氟醚後處理組(Sevo組).I/R組、Ipo組Sevo組採用結扎腸繫膜上動脈60 min,再灌註120min的方法製備腸缺血再灌註模型.Ipo組于再灌註即刻恢複血流30 s後再阻斷30 s,重複3次行後處理.Sevo組于再灌註即刻吸入1.15%七氟醚30 min行後處理.再灌註120 min時,處死大鼠,取小腸組織,採用Chui評分法行病理學損傷評分;採用TUNEL法計算凋亡細胞密度;採用比色法檢測MDA含量和SOD活性;採用Western blot法檢測caspase-3蛋白錶達.結果 與Sham組相比,I/R組、Sevo組和Ipo組病理學損傷評分、凋亡細胞密度和MDA含量均升高,SOD活性降低,caspase-3蛋白錶達上調(P<0.05);與I/R組相比,Sevo組和Ipo組病理學損傷評分、凋亡細胞密度和MDA含量均降低,SOD活性升高,caspase-3蛋白錶達下調(P<0.05);Sevo組和Ipo組病理學損傷評分、凋亡細胞密度、MDA含量、SOD活性和caspase-3蛋白錶達比較差異無統計學意義(P>0.05).結論 七氟醚後處理可通過減輕脂質過氧化反應和減少細胞凋亡,減輕大鼠腸缺血再灌註損傷,其保護效應與缺血後處理相似.
목적 평개칠불미후처리대대서장결혈재관주손상적영향.방법 성년웅성SD대서36지,체중200 ~ 220 g,채용수궤수자표법,장기분위4조(n=9)∶가수술조(Sham조)、장결혈재관주조(I/R조)、결혈후처리조(Ipo조)화칠불미후처리조(Sevo조).I/R조、Ipo조Sevo조채용결찰장계막상동맥60 min,재관주120min적방법제비장결혈재관주모형.Ipo조우재관주즉각회복혈류30 s후재조단30 s,중복3차행후처리.Sevo조우재관주즉각흡입1.15%칠불미30 min행후처리.재관주120 min시,처사대서,취소장조직,채용Chui평분법행병이학손상평분;채용TUNEL법계산조망세포밀도;채용비색법검측MDA함량화SOD활성;채용Western blot법검측caspase-3단백표체.결과 여Sham조상비,I/R조、Sevo조화Ipo조병이학손상평분、조망세포밀도화MDA함량균승고,SOD활성강저,caspase-3단백표체상조(P<0.05);여I/R조상비,Sevo조화Ipo조병이학손상평분、조망세포밀도화MDA함량균강저,SOD활성승고,caspase-3단백표체하조(P<0.05);Sevo조화Ipo조병이학손상평분、조망세포밀도、MDA함량、SOD활성화caspase-3단백표체비교차이무통계학의의(P>0.05).결론 칠불미후처리가통과감경지질과양화반응화감소세포조망,감경대서장결혈재관주손상,기보호효응여결혈후처리상사.
Objective To investigate the effects of sevoflurane postconditioning on intestinal ischemiareperfusion (I/R) injury in rats.Methods Thirty-six adult male Sprague-Dawley rats,weighing 200-220 g,were randomly divided into 4 groups (n =9 each):sham operation group (group Sham),group I/R,ischemic postconditioning group (group Ipo) and sevoflurane postconditioning group (group Sevo).Intestinal I/R was induced by clamping the superior mesenteric artery (SMA) for 60 min followed by 120 min of reperfusion in groups I/R,Ipo and Sevo.In group Ipo the animals were subjected to 3 cycles of 30 min reperfusion-30 min ischemia starting from the beginning of reperfusion.The animals inhaled 1.15% sevoflurane for 30 min starting from the beginning of reperfusion in group Sevo.The animals were sacrificed at 120 min of reperfusion and then the small intestines were removed for determination of malondialdehyde (MDA) content and superoxide dismutase (SOD) activity (by colorimetric method) and caspase-3 protein expression in intestinal tissues (by Western blot).The density of apoptotic cells was calculated by TUNEL.Results Compared with group Sham,the intestinal injury score,density of apoptotic cells and MDA content were significantly increased,SOD activity was decreased,and caspase-3 protein expression was up-regulated in groups I/R,Ipo and Sevo (P < 0.05).Compared with group l/R,the intestinal injury score,density of apoptotic cells and MDA content were significantly decreased,SOD activity was increased,and caspase-3 protein expression was down-regulated in groups Ipo and Sevo (P < 0.05).There was no significant difference in the intestinal injury score,density of apoptotic cells,SOD activity,MDA content and caspase-3 protein expression between Sevo and Ipo groups (P > 0.05).Conclusion Sevoflurane postconditioning can attenuate intestinal I/R injury through reducing lipid peroxidation and cell apoptosis in rats,and the protective effect is similar to that of ischemic post-conditioning.