胰岛素对大鼠缺血随意皮瓣成活的影响

The effects of insulin for enhancement of the viability of the ischemic random flap of rats

目的:观察胰岛素对SD大鼠背部缺血随意皮瓣成活的影响,初步探讨其对皮瓣缺血再灌注损伤的保护作用与提高皮瓣成活率之间的相关性。方法:制备6.0cm×1.5cm的大鼠背部任意皮瓣模型,实验组皮瓣下局部注射胰岛素0.1U(1ml),对照组注射等量生理盐水。测量注射前、注射后1、2、3h血糖浓度,测定24h后皮瓣组织内超氧化物歧化酶(SOD)、谷胱甘肽(GSH)、丙二醛(MDA)含量,测定7天后的皮瓣组织成活率以及免疫组化法测定皮瓣组织微血管的表达。结果:与对照组相比,胰岛素注射组在注射前、注射后1、2、3h的血糖均无显著性差异(P>0.05)。术后24h,胰岛素组的皮瓣组织内的MDA含量显著低于对照组,而GSH、SOD水平显著高于对照组(P<0.05);术后7天,胰岛素组皮瓣的成活率明显高于对照组,(73.963±8.649)%vs(56.175±4.250)%(P<0.01);术后7天,胰岛素组的皮瓣微血管密度明显高于对照组,192.88±42.20vs101.00±22.99(P<0.01)。结论:局部使用胰岛素能明显促进SD大鼠背部缺血任意皮瓣的成活;其机制与降低皮瓣的缺血再灌注损伤有关。

Objective：To investigate insulin on the viability of ischemic random dorsal flap in the SD rats,and discuss the correlation between the protection of the ischemic-reperfusion injury and the enhancement of viability on the random flap of rats . Methods：Rat model with caudally based random dorsal flap measuring 6.0 cm×1.5 cm was constructed,which were divided into 2 groups：treated group（Group A,n=16）with single-dose insulin 0.1 U（1 ml）injection under the flap afer operation and control group（Group B,n=16） with saline. Before injection and 1 h,2 h,3 h after injection,levels of blood glucose were measured. At 24 h postoperatively,the amount of superoxide dismutase（SOD）,glutathione（GSH）and malondialdehyde（MDA）in the flap tissue samples were measured. The flap viability and microvascular expression were measured at 7th day after operation. Results：There was not significant decrease in blood glucose in treated group compared with control group （P 0.05）. At 24 h postoperatively,there was significant decrease in MDA in treated group compared with control group,and significant increase in SOD and GSH （P 0.05）;at 7th day after operation, the viability in treated group was significantly higher compared with that in the control group [（73.963 ±8.649）% vs （56.175 ± 4.250）%,P 0.01]. Conclusion：Topical use of insulin markedly improved the viability of random dorsal flap of SD rats,which may be involved in the reduction of ischemia-reperfusion injury.