南方医科大学学报
南方醫科大學學報
남방의과대학학보
JOURNAL OF SOUTHERN MEDICAL UNIVERSITY
2013年
11期
1685-1688
,共4页
小剂量氯胺酮预处理%气腹%小肠%缺血再灌注损伤
小劑量氯胺酮預處理%氣腹%小腸%缺血再灌註損傷
소제량록알동예처리%기복%소장%결혈재관주손상
low-dose ketamine preconditioning%pneumoperitoneum%small intestine%ischemia reperfusion injury
目的:探讨小剂量氯胺酮预处理对大鼠气腹所致小肠缺血再灌注损伤的保护作用。方法30只健康无特殊病原体级雄性SD大鼠随机分为3组,每组10只。sham组(假手术组,S组,n=10):本组大鼠插管接CO2气腹机,但不充气。model组(模型组,M组,n=10):插管并充气120 min后放气。ketamine组:(氯胺酮预处理组,K组,n=10):气腹前10 min腹腔注射氯胺酮10 mg/kg,插管并充气120 min后放气。同时S组和M组注射等容量的生理盐水。气腹结束后15 min切取小肠组织测定丙二醛(MDA)含量并行病理分析;同时检测血清中肠型脂肪酸结合蛋白(I-FABP)、白介素-6(IL-6)、白介素-8(IL-8)、肿瘤坏死因子α(TNF-α)含量。结果 S组的小肠组织MDA含量明显低于其它两组(P<0.05);且K组肠组织中的MDA含量低于M组大鼠(P<0.05)。与S组相比,K组、M组大鼠血淸I-FABP、IL-6、IL-8、TNF-α含量明显升高(P<0.05);K组明显低于M组(P<0.05)。S组为正常的小肠切片表现;在其他两组小肠黏膜均有不同程度的损伤,病变以M组中最为严重,绒毛结构完整性稍差,排列稍乱,见较多的炎症细胞,粘膜可见充血明显;K组肠黏膜损伤较M组减轻,表现为绒毛顶部脱落减少,少量中性粒细胞浸润。结论小剂量氯胺酮预处理可减轻脂质过氧化反应和抑制促炎性因子释放,对于腹腔镜下气腹所致小肠缺血再灌注损伤有一定的保护作用。
目的:探討小劑量氯胺酮預處理對大鼠氣腹所緻小腸缺血再灌註損傷的保護作用。方法30隻健康無特殊病原體級雄性SD大鼠隨機分為3組,每組10隻。sham組(假手術組,S組,n=10):本組大鼠插管接CO2氣腹機,但不充氣。model組(模型組,M組,n=10):插管併充氣120 min後放氣。ketamine組:(氯胺酮預處理組,K組,n=10):氣腹前10 min腹腔註射氯胺酮10 mg/kg,插管併充氣120 min後放氣。同時S組和M組註射等容量的生理鹽水。氣腹結束後15 min切取小腸組織測定丙二醛(MDA)含量併行病理分析;同時檢測血清中腸型脂肪痠結閤蛋白(I-FABP)、白介素-6(IL-6)、白介素-8(IL-8)、腫瘤壞死因子α(TNF-α)含量。結果 S組的小腸組織MDA含量明顯低于其它兩組(P<0.05);且K組腸組織中的MDA含量低于M組大鼠(P<0.05)。與S組相比,K組、M組大鼠血淸I-FABP、IL-6、IL-8、TNF-α含量明顯升高(P<0.05);K組明顯低于M組(P<0.05)。S組為正常的小腸切片錶現;在其他兩組小腸黏膜均有不同程度的損傷,病變以M組中最為嚴重,絨毛結構完整性稍差,排列稍亂,見較多的炎癥細胞,粘膜可見充血明顯;K組腸黏膜損傷較M組減輕,錶現為絨毛頂部脫落減少,少量中性粒細胞浸潤。結論小劑量氯胺酮預處理可減輕脂質過氧化反應和抑製促炎性因子釋放,對于腹腔鏡下氣腹所緻小腸缺血再灌註損傷有一定的保護作用。
목적:탐토소제량록알동예처리대대서기복소치소장결혈재관주손상적보호작용。방법30지건강무특수병원체급웅성SD대서수궤분위3조,매조10지。sham조(가수술조,S조,n=10):본조대서삽관접CO2기복궤,단불충기。model조(모형조,M조,n=10):삽관병충기120 min후방기。ketamine조:(록알동예처리조,K조,n=10):기복전10 min복강주사록알동10 mg/kg,삽관병충기120 min후방기。동시S조화M조주사등용량적생리염수。기복결속후15 min절취소장조직측정병이철(MDA)함량병행병리분석;동시검측혈청중장형지방산결합단백(I-FABP)、백개소-6(IL-6)、백개소-8(IL-8)、종류배사인자α(TNF-α)함량。결과 S조적소장조직MDA함량명현저우기타량조(P<0.05);차K조장조직중적MDA함량저우M조대서(P<0.05)。여S조상비,K조、M조대서혈청I-FABP、IL-6、IL-8、TNF-α함량명현승고(P<0.05);K조명현저우M조(P<0.05)。S조위정상적소장절편표현;재기타량조소장점막균유불동정도적손상,병변이M조중최위엄중,융모결구완정성초차,배렬초란,견교다적염증세포,점막가견충혈명현;K조장점막손상교M조감경,표현위융모정부탈락감소,소량중성립세포침윤。결론소제량록알동예처리가감경지질과양화반응화억제촉염성인자석방,대우복강경하기복소치소장결혈재관주손상유일정적보호작용。
Objective To investigate the protective effect of low-dose ketamine against intestinal ischemia reperfusion injury following pneumoperitoneum with carbon dioxide in rats. Methods Thirty healthy male adult SD rats (body weight 280-320 g) were randomized into sham-operated group, model group and ketamine group and subjected to pneumoperitoneum for 120 min with carbon dioxide (not in sham-operated group). The rats in ketamine group received an intraperitoneal injection of 10 mg/kg ketamine 10 min before pneumoperitoneum, and those in the other two groups received saline injection. Fifteen minutes after pneumoperitoneum or sham operation, the small intestines were sampled to detect the content of malondialdehyde (MDA) and fore pathological testing. ELISA was used to detect the serum levels of I-FABP, TNF-a IL-6 and IL-8. Results Pneumoperitoneum caused a significant increase in intestinal MDA content (P<0.05), which was lowered by ketamine pretreatment (P<0.05). Serum I- FABP, TNF- a, IL- 6 and IL- 8 levels all significantly increased following pneumoperitoneum (P<0.05) and were obviously lowered by ketamine pretreatment (P<0.05). Pneumoperitoneum also caused obvious pathologies in intestinal mucosa, which were ameliorated by ketamine pretreatment. Conclusion Low-dose ketamine preconditioning can reduce the inflammatory reaction and lessen oxidative damage in the intestinal mucosa following pneumoperitoneum in rats.