外源性-氧化碳对小肠缺血再灌注大鼠不同器官超微结构及细胞凋亡的影响  被引量:4

Effects of exogenous carbon monoxide on ultrastructure changes and apoptosis of different organs induced by intestinal ischemia/reperfusion in rats

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作  者:韩宁[1] 陈卫民[1] 

机构地区:[1]中国医科大学附属盛京医院麻醉科,辽宁省沈阳市110004

出  处:《世界华人消化杂志》2007年第29期3085-3091,共7页World Chinese Journal of Digestology

摘  要:目的:探讨外源性CO对IIR所致多器官损伤的防治作用.方法:♂Wistar大鼠64只,随机分为8组.A组:假手术对照组,不阻断SMA,其余手术过程同其他组:B组:IIR组,吸入空气.C组分为C1亚组与C2亚组,缺血前10 min吸入浓度分别为100μL/L、250μL/L的CO;D组:分为D1亚组与D2亚组,再灌注开始时吸入浓度为100μL/L、250μL/L的CO;E组:分为E1亚组与E2亚组,再灌注60 min时开始吸入浓度为100μL/L、250μL/L的CO.实验结束时取不同组织电镜下观察超微结构变化、TUNEL法荧光显微镜下观察细胞凋亡情况.结果:与A组相比,B组肠和肺组织超微结构损伤严重、凋亡细胞大量出现.而肝组织损伤较轻、肾组织损伤不明显,他们的凋亡细胞数目变化不明显.与B组相比,C、D、E组肠、肺、肝组织超微结构损伤表现轻,C组比D组、E组表现轻,各组内两亚组表现无明显差别.肠和肺组织中凋亡细胞数目从多到少依次是:B组,E1组,E2组,D1组,D2组,C1组,C2纽,A组(P<0.05).结论:外源性CO对大鼠IIR所致多器官损伤具有防治作用,且浓度为250μL/L的CO比100μL/L的CO作用更明显:缺血前应用比缺血及再灌注后应用作用更明显.外源性CO对IIR所致器官损伤的防治作用可能是通过调控细胞凋亡实现的.AIM: To investigate the effects of CO on multiple organ injury induced by intestinal ischemia/ reperfusion (IIR) in rats. METHODS: Sixty-four male Wistar rats, weighing 220-260 g, were randomly allocated into eight groups with eight animals in each. The model of IIR was established by clamping the superior mesenteric artery (SMA) for 60 rain and reperfusion for 120 rain. Group A, sham operation, no SMA clamping; group B, SMA clamping for 60 min and reperfusion for 120 min; group C1/C2, inhaled 100 μL/L/250 μL/L CO 10 min before SMA clamping; group D1/D2, inhaled 100 μL/L/250 μL/L CO 60 min after SMA clamping; group El/E2, inhaled 100 μL/L/250 μL/L CO 60 min after reperfusion. The ultrastructure of different tissues was observed by transmission electron microscopy, and apoptosis of different cells was determined by terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL). RESULTS: The extent of ultrastructural damage in the different tissues in group B was intestinal 〉 lung 〉 liver, with no significant change in the kidneys; and in different groups, it was group C 〈 D 〈 E 〈 B, with no significant differences between the 250 AL/L and 100 AL/L groups. Few apoptotic cells were seen in the liver and kidneys, but many in the intestine and lungs; and in different groups, the number of apoptotic cells was group A 〈 C2 〈 C1 〈 D2 〈 D1 〈 E2 〈 E1 〈 B (P 〈 0.05). CONCLUSION: Exogenous CO can provide protection against multiple organ injury induced by IIR in rats. The effect of 250 μL/L CO is more significant than that of 100 μL/L CO, and the effect of CO is more significant when it is used before intestinal ischemia than after. Exogenous CO provides protection against multiple organ injury induced by IIR, partly through modulating apoptosis.

关 键 词:一氧化碳 小肠 缺血再灌注 超微结构 凋亡 TUNEL法 

分 类 号:R363[医药卫生—病理学]

 

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