| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2018: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2017: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2016: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2015: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
|
|---|
| Outline of Final Research Achievements |
AIM: To demonstrate neuronal mechanisms underlying ischemic pain with peripheral arterial disease (PAD), we investigated the role of NGF and VEGF on muscle hyperalgesia and intermittent claudication in a rat model of PAD. METHODS: We ligated the left common iliac and iliolumbar arteries completely. NGF and VEGF proteins in the gastrocnemius muscle (GM) were measured respectively. Effects of inhibitor of TrkA, a receptor of NGF, and VEGFR2, a receptor of VEGF were evaluated on behavioral responses. The expression of TrkA- and VEGFR2-receptor were examined in DRG neurons innervating GM. RESULT: We found muscle hyperalgesia and intermittent claudication after ligation. NGF protein level increased in GM and intramuscular injection of either TrkA- and VEGFR2-inhibitor suppressed muscle hyperalgesia in PAD rats. CONCLUSION:NGF and VEGF may play an important role in developing muscle hyperalgesia associated with PAD.
|
