CAJ | 학술논문

目的：探讨超声空化微泡效应促进缺血骨骼肌血管新生的作用及可能机制。方法：30只Wister大鼠离断右侧股动脉后7 d 随机平均分为3组：超声＋微泡组（A 组）、超声组（B 组）、对照组（C组）。实验结束后，各组分别取1只大鼠骨骼肌做石蜡切片观察显微结构的变化。各组剩余的大鼠分别于24 h及7 d后处死，检测炎症因子E-选择素（E-selectin）、单核细胞趋化因子-1（MCP-1）和骨骼肌组织中血管内皮生长因子（VEGF）表达情况。结果：A 组骨骼肌中 VEGF 表达较多，有较多的新生血管生成，同时 E-selectin 及MCP-1的表达量较其他两组也相应增加（P＜0．05）；而 B 组及 C 组 VEGF 表达较少，炎症因子表达量也较少。结论：超声空化微泡效应引起的微血管破裂可通过刺激骨骼肌中内源性VEGF 的分泌，促进血管生成，同时炎症因子表达量增加可能是其机制之一。
목적：탐토초성공화미포효응촉진결혈골격기혈관신생적작용급가능궤제。방법：30지Wister대서리단우측고동맥후7 d 수궤평균분위3조：초성＋미포조（A 조）、초성조（B 조）、대조조（C조）。실험결속후，각조분별취1지대서골격기주석사절편관찰현미결구적변화。각조잉여적대서분별우24 h급7 d후처사，검측염증인자E-선택소（E-selectin）、단핵세포추화인자-1（MCP-1）화골격기조직중혈관내피생장인자（VEGF）표체정황。결과：A 조골격기중 VEGF 표체교다，유교다적신생혈관생성，동시 E-selectin 급MCP-1적표체량교기타량조야상응증가（P＜0．05）；이 B 조급 C 조 VEGF 표체교소，염증인자표체량야교소。결론：초성공화미포효응인기적미혈관파렬가통과자격골격기중내원성VEGF 적분비，촉진혈관생성，동시염증인자표체량증가가능시기궤제지일。
Objective To investigate the role and possible mechanism of ultrasound-targeted microbubble destruction for accelerating neovascularisation in ischemic skeletal muscle. Methods Unilateral hind limb ischaemia was surgically induced in thirty wister rats. On postoperative day 7 , the rats were randomly divided into three groups: ultrasound-targeted microbubble destruction group (group A), ultrasound group (group B), and control group. After the end of the experiment , parafin sections for the skeletal muscle from one rat in each group were made to observe the changes in microstructure. The remaining rats were sacrificed at 24 h and on day 7. VEGF expression, inflammatory factor E-selectin, and monocyte chemotactic factor-1 (MCP-1) were detected in the rats. Results As compared with the other two goups, expressions of VEGF, neovascularization, E-selectin, and MCP-1 in the skeletal muscle were significantly increased in group A. Conclusions Microvascular rupture caused by ultrasound-targeted microbubble destruction can promote angiogenesis by stimulating secretion of endogenous VEGF in skeletal muscle; meanwhile, an increase in expression level of inflammatory factors may be one of the mechanisms.