摘要
目的探讨低压稳恒直流电场对兔梗死-缺血心肌毛细血管新生的效应。方法将健康中国家兔40只分为心肌梗死(myocardial infarction,MI)组、平面电场2.0V组、平面电场3.0V组、透壁电场2.0V组和透壁电场3.0V组。4周后对梗死部位心肌组织进CD31免疫组织化学染色检测毛细血管密度。结果透壁电场缩小梗死面积优于平面电场;透壁电场3.0V可显著促进毛细血管新生和形成,尤以非梗死区明显。结论适宜的低压稳恒直流电场具有促进兔MI/缺血模型心肌毛细血管新生的作用。
Objective To investigate whether there is therapeutic angiogenic responses in ischemic myocardium of rabbit injured and chronic infracted heart under the weak steady direct current electrical fields (DCEFs) of 2.0 and 3.0 V/cm. Methods Forty Chinese rabbits established as myocardial infarction model without endotracheal intubation were randomly divided into 5 groups, i. e. , myocardial infarction (MI) group, plane electrical fields of 2.0 V (PEF2V) group, the plane electrical fields of 3.0 V (PEF3V) group, transmural electrical fields of 2.0 V (TEF2V) group, and transmural electrical fields of 3.0 V (TEF3V) group. Either plane or transmural DCEFs of 2.0 V or 3.0 V were applied to ischemic myocardium of rabbit models of chronic myocardial infarction. After g weeks, histopathological analyses were performed to evaluate the efficacy of the weak steady DCEFs applied on the surface of ischemic myocardium. Results Significant improvement was found in minimizing infarct area and lowering the extent of fibrosis among the g applied DCEFs groups, and the transmural electrical fields were superior to the plane electrical fields. Additionally, more CD31-immunostained vessels were also found in infarcted area, border zone infarcted area, and noninfarcted area in TEF3V group than that in the other groups, but predominant in noninfarcted area. Conclusion These preliminary results indicate that the eligible weak steady DCEFs applied on the surface of ischemic myocardium induces angiogenesis and possibly collateral circulation in ischemic myocardium, thereby protecting the myocardium.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2008年第5期402-405,共4页
Journal of Third Military Medical University
基金
国家自然科学基金(30470452)~~
关键词
电场
稳恒直流
冠状动脉
心肌梗死
血管新生
direct current electrotherapy
coronary artery
myocardial infarction
therapeutic angiogenesis
cardiac function