论文部分内容阅读
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 observe the effect of insulin on the survival of ischemic free flaps in SD rats and to investigate the correlation between the protection of flaps against ischemia-reperfusion injury and the survival rate of flaps. Methods: An arbitrary skin flap model of 6.0 cm × 1.5 cm in the back of rats was prepared. Insulin 0.1 U (1 ml) was injected under the flap of the experimental group, and the control group was injected with the same amount of saline. Blood glucose levels were measured at 1, 2 and 3 hours after injection. The contents of superoxide dismutase (SOD), glutathione (GSH) and malondialdehyde (MDA) Survival rate of flap tissue and immunohistochemistry were used to determine the expression of microvascular in flap tissue. Results: Compared with the control group, there was no significant difference in the blood glucose level between the two groups before and 1, 2 and 3 hours after injection (P> 0.05). The level of MDA in the skin tissue of the insulin group was significantly lower than that of the control group at 24 hours after operation, while the levels of GSH and SOD were significantly higher than those in the control group (P <0.05). At 7 days after operation, the survival rate of the flap in the insulin group was significantly higher (73.963 ± 8.649)% vs (56.175 ± 4.250)% (P <0.01). In the 7th day after operation, the microvessel density in the insulin group was significantly higher than that in the control group (192.88 ± 42.20vs101.00 ± 22.99) P <0.01). CONCLUSION: Topical application of insulin can significantly promote the survival of any flaps in the back of SD rats. The mechanism is related to the reduction of the ischemia-reperfusion injury of the flaps.