Does acute pain progress to chronic pain: mechanisms of persistent postoperative pain

2015 Fiscal Year Final Research Report

• Project/Area Number: 24390365
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Anesthesiology/Resuscitation studies
• Research Institution: Shinshu University
• Principal Investigator: KAWAMATA Mikito 信州大学, 学術研究院医学系, 教授 (90315523)
• Co-Investigator(Kenkyū-buntansha): TANAKA Satoshi 信州大学, 学術研究院医学系, 准教授 (60293510) ; SUGIYAMA Yuki 信州大学, 学術研究院医学系, 助教 (10468100) ; ISHIDA Takashi 信州大学, 医学部附属病院, 助教(診療) (60531952) ; SUGIYAMA Daisuke 信州大学, 医学部, 助教(特定雇用) (40467189) ; KAWAMATA Tomoyuki 信州大学, 医学部, 准教授 (80336388)
• Project Period (FY): 2012-04-01 – 2016-03-31
• Keywords: 術後痛 / 遷延性術後痛 / 動物モデル / 筋肉 / 慢性炎症 / マイクログリア

Outline of Final Research Achievements

We hypothesized that muscle injury with persistent inflammation would induce persistent postoperative pain (PPOP). We prepared two types of muscle injury, plantar muscle incision and plantar muscle cryoinjury caused by liquid nitrogen of the rat hind paw. Plantar muscle cryoinjury induced greater mechanical hyperalgesia from day 5 to 8 and spontaneous pain from day 3 to 7 compared with plantar muscle incision. In plantar muscle cryoinjury, the number of inflammatory cells in injured muscle and spinal Iba-1 expression were significantly higher compared with those in plantar muscle incision. Taken together, plantar muscle cryoinjury is a more appropriate model of PPSP compared with plantar muscle incision. This model effectively reflected the characteristics of PPSP. In addition, the results of this study suggest that spinal microglial activation is involved in the pathogenic mechanism of PPOP.

Free Research Field

麻酔蘇生学