摘要
目的探讨利多卡因对大鼠皮瓣缺血-再灌注损伤的保护作用及机制。方法将36只成年SD大鼠随机平均分成对照组、假处理组和利多卡因组。制取5 cm×4 cm上腹部岛状皮瓣后,假处理组不作缺血-再灌注处理而直接原位缝合;缺血9 h后,利多卡因组于再灌注前5 min腹腔内注射10mg/kg利多卡因,对照组则注射1 ml生理盐水。再灌注后12 h测定皮瓣组织丙二醛水平和髓过氧化物酶水平,并在术后1周观察3组皮瓣成活情况。结果7 d后利多卡因组皮瓣成活率为74.31%,对照组为27.23%,假处理组为98.23%,利多卡因组和对照组皮瓣成活率有显著性差异(P<0.05)。利多卡因组丙二醛水平为6.12 nmol/g,对照组为11.64 nmol/g,假处理组为6.01 nmol/g,利多卡因组与对照组丙二醛水平存在显著差异(P<0.05)。利多卡因组髓过氧化物酶水平为120.23 U/g,对照组为128.45 U/g,假处理组为80.31 U/g,利多卡因组和对照组间无显著性差异(P>0.05)。结论利多卡因能有效抑制和阻断缺血-再灌注损伤相关的自由基团释放、超氧化物阴离子生成,减少脂质产物降解,从而有效提高皮瓣成活。
Objective To investigate the effect and underlying mechanisms of lidocaine to protect flap of rat following ischemia reperfusion injury. Methods Thirty-six S-D rats were devided into 3 groups averagely and randomly as control, sham and lidocaine group. After a 5 cm× 4 cm epigastric flap elevated, the flaps of sham group were again sutured into its place without inducing any ischaermia. Following a 9 hour isehemic period and 5 min prior to the reperfusion, 1 ml saline was injected via intraperitoneal route in the control group, while the lidocaine group was injected 10 mg/kg lidocaine. Following a 12 hour reperfusion, the level of malonaldehyde and myeloperoxidase of the flap tissue were evaluated. And the flap survival rate was evaluated in the 7th day post reperfusion. Results The flap survival rate of 7th day post-repurfusion was 74. 31% in the lidocaine group, 27.23% in the control group and 98. 23% in the sham group, there was a significance difference between the lidocaine group and control group （P〈0.05）. The level of malonaldehyde was 6. 12 nmol/g in the lidocaine group, 11.64 nmol/g in the control group and 6.01 nmol/g in the sham group, there was also a significance difference between lidocaine group and control group （P〈0. 05）. The level of myeloperoxidase was 120. 23 U/g in the lidoeaine group, 128.45 U/g in the control group and 80. 31 U/g in the sham group, there was no significance differences between lidocaine group and control group （P〉 0. 05）. Conclusion Lidocaine effectively elevate the flap survival rate by inhibiting and blocking the release of free radical, the production of superoxide anion and ruducing lipid degradation associated with ischemia-reperfusion injury.
出处
《国际骨科学杂志》
2010年第2期125-127,共3页
International Journal of Orthopaedics
