中国医师杂志
中國醫師雜誌
중국의사잡지
JOURNAL OF CHINESE PHYSICIAN
2008年
12期
1598-1601
,共1页
邹晓防%吴绍卫%周国勇%胡森%吕艺%黎君友%盛志勇
鄒曉防%吳紹衛%週國勇%鬍森%呂藝%黎君友%盛誌勇
추효방%오소위%주국용%호삼%려예%려군우%성지용
卡巴胆碱/药理学%再灌注损伤%炎症%肿瘤坏死因子α%血量
卡巴膽堿/藥理學%再灌註損傷%炎癥%腫瘤壞死因子α%血量
잡파담감/약이학%재관주손상%염증%종류배사인자α%혈량
Carbachol/PD%Reperfusion injury%Inflammation%Tumor necrosis factor-alpha%Blood volume
目的 研究缺血再灌流时卡巴胆碱对缺血再灌流大鼠肠组织炎症反应和血流量的影响.方法 Wistar大鼠开腹制做空肠袋,夹闭肠系膜上动脉(SMA)阻断血流45 min后恢复血流,制成肠缺血-再灌流模型.动物随机分为假手术组、缺血-再灌流+生理盐水组(I/R+NS)和缺血-再灌流+卡巴胆碱组(I/R+Ca).I/R+Ca组在SMA阻断血流同时向肠袋内注射卡巴胆碱(0.1mg/kg),I/R+NS组给予相同剂量的生理盐水.观察肠黏膜损伤情况;检测肠组织中DAO含量;ELLSA法测定肠组织中TNF-α含量;应用多普勒血流仪测定肠黏膜血流量.结果 I/R+Ca组与I/R+NS组相比,肠黏膜病理变化较轻.I/R+Ca组肠袋黏膜组织DAO活性较L/R+NS组显著增加(P<0.01);同时L/R+Ca组与I/R+NS组相比,肠黏膜血流量明显增加(P<0.01),而肠I/R+Ca组黏膜组织中TNF-α含量较I/R+Ns明显减少(P<0.01).结论 卡巴胆碱能促进缺血再灌流时肠黏膜血流恢复,增加肠黏膜血流量;抑制肠组织中TNF-α的生成,减轻肠黏膜病理损害,时肠黏膜具有保护作用.
目的 研究缺血再灌流時卡巴膽堿對缺血再灌流大鼠腸組織炎癥反應和血流量的影響.方法 Wistar大鼠開腹製做空腸袋,夾閉腸繫膜上動脈(SMA)阻斷血流45 min後恢複血流,製成腸缺血-再灌流模型.動物隨機分為假手術組、缺血-再灌流+生理鹽水組(I/R+NS)和缺血-再灌流+卡巴膽堿組(I/R+Ca).I/R+Ca組在SMA阻斷血流同時嚮腸袋內註射卡巴膽堿(0.1mg/kg),I/R+NS組給予相同劑量的生理鹽水.觀察腸黏膜損傷情況;檢測腸組織中DAO含量;ELLSA法測定腸組織中TNF-α含量;應用多普勒血流儀測定腸黏膜血流量.結果 I/R+Ca組與I/R+NS組相比,腸黏膜病理變化較輕.I/R+Ca組腸袋黏膜組織DAO活性較L/R+NS組顯著增加(P<0.01);同時L/R+Ca組與I/R+NS組相比,腸黏膜血流量明顯增加(P<0.01),而腸I/R+Ca組黏膜組織中TNF-α含量較I/R+Ns明顯減少(P<0.01).結論 卡巴膽堿能促進缺血再灌流時腸黏膜血流恢複,增加腸黏膜血流量;抑製腸組織中TNF-α的生成,減輕腸黏膜病理損害,時腸黏膜具有保護作用.
목적 연구결혈재관류시잡파담감대결혈재관류대서장조직염증반응화혈류량적영향.방법 Wistar대서개복제주공장대,협폐장계막상동맥(SMA)조단혈류45 min후회복혈류,제성장결혈-재관류모형.동물수궤분위가수술조、결혈-재관류+생리염수조(I/R+NS)화결혈-재관류+잡파담감조(I/R+Ca).I/R+Ca조재SMA조단혈류동시향장대내주사잡파담감(0.1mg/kg),I/R+NS조급여상동제량적생리염수.관찰장점막손상정황;검측장조직중DAO함량;ELLSA법측정장조직중TNF-α함량;응용다보륵혈류의측정장점막혈류량.결과 I/R+Ca조여I/R+NS조상비,장점막병리변화교경.I/R+Ca조장대점막조직DAO활성교L/R+NS조현저증가(P<0.01);동시L/R+Ca조여I/R+NS조상비,장점막혈류량명현증가(P<0.01),이장I/R+Ca조점막조직중TNF-α함량교I/R+Ns명현감소(P<0.01).결론 잡파담감능촉진결혈재관류시장점막혈류회복,증가장점막혈류량;억제장조직중TNF-α적생성,감경장점막병리손해,시장점막구유보호작용.
Objective To investigate the effects of carbachol on intestinal inflammation and mucosal blood flow after gut ischemia-repedusion(I/R) in rat. Method A jejunal sac was formed in Wistar rats. The superior mesenteric artery (SMA) was occluded for 45 mi-nutes followed by 240 minutes of reperfusion. Animals were random divided into three groups: sham operation, L/R + saline injection (I/R + NS) and I/R + carbachol injection (0.1mg/kg, I/R + Ca). Immediately after occluded of SAM blood flow, either 0.1mg/kg of carba-chol or same account of 0.9% saline was injected into the jejunal sac. The pathological injury was observed with HE staining. The activity of DAO and content of TNF-α in intestinal mucosa tissue were determined. Mucosal blood flow was measured by laser Doppler. All measure-ments were done at 0 min, 30 min, 60 min, 120 min, and 240 min after reperfusion. Result In I/R group the activity of DAO in intestinal mucosa and mucosal blood flow deceased, meanwhile the content of TNF-α gut tissue was dramatically increased than those in sham operation (P<0.01). Severe pathological changes were observed in intestinal mucosa. After injection of carbachol, the activity of DAO and mucosal blood flow increased (P<0.01), but the content of TNF-α in intestinal mucosa were dramatically decreased (P<0.01), compared with those in I/R group. Conclusion Administration of carbachol protects intestinal ischemia-reperfusion injury by attenuating intestinal mucosa inflammation and increasing gut mueosal blood flow.