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作 者:史继德[1] 康博雄[1] 张代成[1] 晏波[1] 王秉钧[1] 马仁军[2] 王世文[1] 詹乐恒[1]
机构地区:[1]兰州大学第二医院急救中心外科,甘肃兰州730030 [2]兰州大学校医院,甘肃兰州730000
出 处:《兰州大学学报(医学版)》2006年第1期4-6,10,共4页Journal of Lanzhou University(Medical Sciences)
摘 要:目的探讨糖皮质激素在失血性休克中,对肠组织细胞间粘附分子-1及肠屏障功能的影响。方法新西兰大白兔30只,随机分为失血性休克组、甲基强的松龙处理组和正常对照组。失血性休克采用股动脉放血制作模型,休克持续2h后回输失血及等量林格氏液复苏;甲基强的松龙组在复苏时静注1次甲基强的松龙50 mg/kg;对照组不行放血处理。各组复苏后2 h,取小肠组织行常规病理学检查,并制备肠组织匀浆,采用ELISA法测定细胞间粘附分子-1(ICAM-1);检测肠组织匀浆髓过氧化物酶(MPO)活性;留取血浆检测D-乳酸水平。结果与失血性休克组比较,甲基强的松龙处理组小肠组织中ICAM-1及MPO均降低,肠粘膜损伤程度轻,血浆D-乳酸水平也低。结论早期大剂量运用甲基强的松龙,能够抑制失血性休克后肠组织ICAM-1的表达,减轻肠结构的破坏,保护肠粘膜屏障功能。Objective To investigate the influence of methylprednisolone on intestinal tissue ICAM-1 in intestinal barrier dysfunction after hemorrhagic shock of rabbits. Methods Thirty rabbits were randomly divided into three groups: control groups, hemorrhagic shock group and methylprednisolone-treatment group. Hemorrhagic shock was induced by modified Wiggets method until mean arterial pressure was stabilized within the range of 35 to 40 mmHg. The hypotension was maintained for 2 hours before lost blood and equivalent amount of Ringer's solution were infused. 50 mg/kg of methylprednisolone was given when methylprednisolone treatment group began to resuscitate. At 60 min after reperfusion, rabbits were decapitated. The levels of ICAM-1 and the activity of MPO in intestine homogenates-were determined. At the same time, the content of D-lactate in the plasma was determined and pathological changes in intestinal were observed. Results Compared with control group, ICAM-1, MPO and D-lactate were significantly increased in hemorrhagic shock group and they reversed to some degrees with the treatment of methylprednisolone. The histopathologic results were consistent with the biochemical markers. Conclusion Methylprednisolone can inhibit the expression of ICAM-1 in intestinal tissue and has potential protective effects on the intestinal barrier function after hemorrhagic shock.
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