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The elucidation of the mechanisms of cardiovascular hypertrophy and hyperplasia and the establishment of angiogenesis by therapeutic electrical stimulation

阐明心血管肥大和增生的机制以及通过治疗性电刺激建立血管生成

基本信息

批准号：
12670643
负责人：
KOHZUKI Masahiro
金额：
$ 2.18万
依托单位：
Tohoku University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2000
资助国家：
日本
起止时间：
2000 至 2001
项目状态：
已结题

项目摘要

Low voltage electrical stimulation (LVES) of skeletal muscle at a level far below the threshold of muscle contraction has been reported to induce synthesis of VEGF. We examined whether LVES induced VEGF production in hindlimb ischemia model of rats was due to hypoxia or inflammation. We also tried to evaluate whether other angiogenic factors, such as hepatocyte growth factor (HGF) and fibroblast growth factor (FGF), also contribute to the local angiogenesis by LVES. Thirdly we compared the effect of LVES with that of high VES (HVES) on the induction of angiogenic factors.Not only VEGF but also HGF was significantly increased in tissues by LVES. There was no difference in the level of immunohistochemical staining of the tibialis anterior (TA) muscles with polyclonal anti FGF antibody, anti IL6 antibody, and HIF antibody between the LVES group and control group. The VEGF level of the intermittent HVES group tended to be higher than that of the continuous LVES or intermittent LVES groups although the difference was not significant. Therefore, not only VEGF but also HGF may contribute to the local angiogenesis by LVES in this model. It was also demonstrated that the LVES-induced VEGF production in this model may not be due to hypoxia or inflammation by LVES. Thirdly, we demonstrated that the induction of VEGF by LVES was seen at a significantly earlier period than that by HVES and that the increase in the ratio of VEGF synthesis of stimulated to control by LVES was smaller than that by HVES comparing between 1 day and 5 days.In conclusion, continuous LVES in a hindlimb ischemia model of rats was effective for VEGF and HGF induction which was not seen on high voltage stimulation, and ES might be useful for ischemic disease even at low voltage.

据报道，远低于肌肉收缩阈值的骨骼肌低压电刺激（LVES）可诱导VEGF合成。我们观察LVES诱导大鼠后肢缺血模型中VEGF的产生是由于缺氧还是炎症。我们还试图评估其他血管生成因子，如肝细胞生长因子（HGF）和成纤维细胞生长因子（FGF）是否也有助于LVES局部血管生成。第三，比较低氧和高氧（HVES）对血管生成因子的诱导作用。LVES不仅使VEGF显著升高，而且使HGF显著升高。LVES组与对照组大鼠胫骨前肌（TA）多克隆抗FGF抗体、抗IL6抗体和HIF抗体的免疫组化染色水平无差异。间歇HVES组VEGF水平有高于连续LVES组和间歇LVES组的趋势，但差异无统计学意义。因此，在该模型中，除了VEGF外，HGF也可能参与LVES的局部血管生成。该模型中LVES诱导的VEGF生成可能不是由于LVES缺氧或炎症所致。第三，我们发现LVES诱导VEGF的时间明显早于HVES，并且在第1天和第5天，LVES刺激与对照的VEGF合成比例的增加幅度小于HVES。综上所述，在大鼠后肢缺血模型中，连续LVES对VEGF和HGF的诱导是有效的，这是高压刺激所没有的，即使在低电压下，ES也可能对缺血性疾病有用。