Contribution of stress-induced hypercatecholamine state for the development of postoperative chronic pain

2020 Fiscal Year Final Research Report

• Project/Area Number: 17K16746
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Anesthesiology
• Research Institution: Kyoto Prefectural University of Medicine
• Principal Investigator: Yamasaki Masaki 京都府立医科大学, 医学(系)研究科(研究院), 助教 (20771520)
• Project Period (FY): 2017-04-01 – 2021-03-31
• Keywords: 高カテコラミン血症

Outline of Final Research Achievements

Catecholamine-degrading enzyme COMT inhibitor was administered intraperitoneally. Behavioral analysis showed that hyperalgesia developed in the hypercatecholaminergic model. beta2 adrenergic receptors are expressed in small neurons of the dorsal root ganglia and their expression was increased in the hypercatecholaminergic model. The beta2 adrenergic receptor antagonists had no apparent effect on hyperalgesia caused by hypercatecholaminemia. GRK2, which is involved in the regulation of receptor signaling, tended to increase in the hypercatecholaminergic model, but the change was not statistically significant.

Free Research Field

疼痛治療学

Academic Significance and Societal Importance of the Research Achievements

慢性ストレスは放置すると慢性痛を引き起こしやすく、ストレス誘引性の慢性痛は原因が明らかでなく難治性である。持続的な高カテコラミン血症は慢性ストレス疾患によく観察される症状の一つである。本研究において、高カテコラミン血症が痛覚閾値に影響をあたえ痛覚過敏を誘発することが示された結果、ストレス誘引性慢性痛の治療法に新しい視点を提供することができた。今後、高カテコラミン血症が痛覚過敏を引き起こす分子メカニズムの解明を行う予定である。