中华普通外科杂志
中華普通外科雜誌
중화보통외과잡지
CHINESE JOURNAL OF GENERAL SURGERY
2011年
4期
328-331
,共4页
缺血%再灌注损伤%疾病模型,动物%运动障碍%胞间黏附分子1
缺血%再灌註損傷%疾病模型,動物%運動障礙%胞間黏附分子1
결혈%재관주손상%질병모형,동물%운동장애%포간점부분자1
Ischemia%Reperfusion injury%Disease models,animal%Movement disorders%Intercellular adhesion molecule-1
目的 探讨肠缺血再灌注(intestinal ischemia reperfusion,IIR)损伤大鼠小肠运动功能的变化及其与细胞间黏附分子1(intercellular adhesion molecule-1,ICAM-1)表达的关系.方法 将Wistar大鼠30只随机分为ⅡR组、ICAM-1单抗组和假手术组,ⅡR组采用夹闭-放开肠系膜上动脉的方法建立IIR损伤模型,ICAM-1单抗组于阻断肠系膜上动脉血供同时静脉给予ICAM-1单克隆抗体1 mg/kg.用荧光分光光度法测定各组大鼠小肠传输功能,多导生理仪测定环行肌条收缩能力的变化,RT-PCR法检测小肠肌层ICAM-1 mRNA的表达量,免疫组化法检测ICAM-1蛋白表达,图像分析系统计数小肠肌层浸润白细胞数量,比色法测定小肠肌层组织髓过氧化物酶(myeloperoxidase,MPO)的活性.结果 ICAM-1单抗组较ⅡR组大鼠小肠传输功能明显改善,几何中心分别为8.4±0.7和3.4±0.5;两组环形平滑肌条收缩力为(1.81±0.28)g/mm2·s-1和(0.52±0.09)g/mm2·s-1;浸润白细胞数量为(5.6±2.2)c/f和(18.2±3.1)c/f;MPO活性为(2.03±0.56)U/g和(6.41±1.25)U/g,两组各项指标之间比较差异均有统计学意义(P＜O.05).两组小肠肌层ICAM-1 mRNA的表达量为1.69±0.57和1.76±0.32,差异无统计学意义(P＞0.05).IIR组和ICAM-1单抗组小肠肌层均有大量棕色颗粒样染色.结论IIR损伤上调小肠肌层ICAM-1 mRNA的表达,介导中性粒细胞的黏附和浸润,导致小肠运动功能的障碍.
目的 探討腸缺血再灌註(intestinal ischemia reperfusion,IIR)損傷大鼠小腸運動功能的變化及其與細胞間黏附分子1(intercellular adhesion molecule-1,ICAM-1)錶達的關繫.方法 將Wistar大鼠30隻隨機分為ⅡR組、ICAM-1單抗組和假手術組,ⅡR組採用夾閉-放開腸繫膜上動脈的方法建立IIR損傷模型,ICAM-1單抗組于阻斷腸繫膜上動脈血供同時靜脈給予ICAM-1單剋隆抗體1 mg/kg.用熒光分光光度法測定各組大鼠小腸傳輸功能,多導生理儀測定環行肌條收縮能力的變化,RT-PCR法檢測小腸肌層ICAM-1 mRNA的錶達量,免疫組化法檢測ICAM-1蛋白錶達,圖像分析繫統計數小腸肌層浸潤白細胞數量,比色法測定小腸肌層組織髓過氧化物酶(myeloperoxidase,MPO)的活性.結果 ICAM-1單抗組較ⅡR組大鼠小腸傳輸功能明顯改善,幾何中心分彆為8.4±0.7和3.4±0.5;兩組環形平滑肌條收縮力為(1.81±0.28)g/mm2·s-1和(0.52±0.09)g/mm2·s-1;浸潤白細胞數量為(5.6±2.2)c/f和(18.2±3.1)c/f;MPO活性為(2.03±0.56)U/g和(6.41±1.25)U/g,兩組各項指標之間比較差異均有統計學意義(P＜O.05).兩組小腸肌層ICAM-1 mRNA的錶達量為1.69±0.57和1.76±0.32,差異無統計學意義(P＞0.05).IIR組和ICAM-1單抗組小腸肌層均有大量棕色顆粒樣染色.結論IIR損傷上調小腸肌層ICAM-1 mRNA的錶達,介導中性粒細胞的黏附和浸潤,導緻小腸運動功能的障礙.
목적 탐토장결혈재관주(intestinal ischemia reperfusion,IIR)손상대서소장운동공능적변화급기여세포간점부분자1(intercellular adhesion molecule-1,ICAM-1)표체적관계.방법 장Wistar대서30지수궤분위ⅡR조、ICAM-1단항조화가수술조,ⅡR조채용협폐-방개장계막상동맥적방법건립IIR손상모형,ICAM-1단항조우조단장계막상동맥혈공동시정맥급여ICAM-1단극륭항체1 mg/kg.용형광분광광도법측정각조대서소장전수공능,다도생리의측정배행기조수축능력적변화,RT-PCR법검측소장기층ICAM-1 mRNA적표체량,면역조화법검측ICAM-1단백표체,도상분석계통계수소장기층침윤백세포수량,비색법측정소장기층조직수과양화물매(myeloperoxidase,MPO)적활성.결과 ICAM-1단항조교ⅡR조대서소장전수공능명현개선,궤하중심분별위8.4±0.7화3.4±0.5;량조배형평활기조수축력위(1.81±0.28)g/mm2·s-1화(0.52±0.09)g/mm2·s-1;침윤백세포수량위(5.6±2.2)c/f화(18.2±3.1)c/f;MPO활성위(2.03±0.56)U/g화(6.41±1.25)U/g,량조각항지표지간비교차이균유통계학의의(P＜O.05).량조소장기층ICAM-1 mRNA적표체량위1.69±0.57화1.76±0.32,차이무통계학의의(P＞0.05).IIR조화ICAM-1단항조소장기층균유대량종색과립양염색.결론IIR손상상조소장기층ICAM-1 mRNA적표체,개도중성립세포적점부화침윤,도치소장운동공능적장애.
Objective To evaluate the relationship between the intestinal motility alterations and intercellular adhesion molecule-1 ( ICAM-1 ) expression within the rat intestinal muscularis after ischemia reperfusion. Methods Thirty Wistar rats were divided randomly into IIR, monoclanal anti-ICAM-1 and sham group (n = 10), HR models were established by clamping-releasing the superior mesenteric artery. Gut transit was measured in vivo and intestinal circular muscle contractions were measured in an organ bath. The expression of ICAM-1 mRNA was detected by RT-PCR and immunohistochemisty. Leukocyte infiltration and myeloperoxidase (MPO) activity were quantified in sham and ischemia/reperfusion rats with and without monoclonal anti-ICAM-1 antibody treatment. Results The gut transit of monoclonal anti-ICAM-1 group was improved obviously as compared with IIR group. Circular smooth muscle contractility stimulated by ICAM-1 mRNA expression was 1.69 ± 0. 57 and 1.76 ± 0. 32 within the muscularis; Leukocyte infiltration into the muscularis was (5.6 ±2. 2) c/f and ( 18. 2 ±3. 1 ) c/f. MPO activity was (2. 03 ±0. 56) U/g and (6. 41 ± 1.25 ) U/g respectively. The differences were all statistically significant between IIR and treatment groups ( P ＜ 0. 05 ). The expression of ICAM-1 protein in IIR and anti-ICAM-1 groups was not significantly different (P ＞ 0. 05). Conclusions The up-regulated expression of ICAM-1 after ⅡR injury calls forth local infiltration of PMN within the intestinal muscularis, leading to intestinal motility dysfunction.
