HMGB1-induced vaspressin deficiency contributes to septic shock

2014 Fiscal Year Final Research Report

• Project/Area Number: 24390402
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Emergency medicine
• Research Institution: Kagoshima University
• Principal Investigator: ITO Takashi 鹿児島大学, 医歯(薬)学総合研究科, 講師 (20381171)
• Co-Investigator(Kenkyū-buntansha): MARUYAMA Ikuro 鹿児島大学, 大学院医歯学総合研究科, 特任教授 (20082282)
• Co-Investigator(Renkei-kenkyūsha): NAKAHARA Mayumi 鹿児島大学, 大学院医歯学総合研究科, 特任助教 (90707514) ; KAWAHARA Ko-ichi 大阪工業大学, 工学部生命工学科, 特任教授 (10381170)
• Research Collaborator: NAGASATO Tomoka 藤森工業株式会社 ; YAMADA Shingo 株式会社シノテスト ; TAKENAKA Yukari 鹿児島大学, 大学院医歯学総合研究科
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 敗血症性ショック / バソプレシン / HMGB1 / DAMPs

Outline of Final Research Achievements

Vasopressin deficiency contributes to the vasodilatation in the later stages of septic shock, and supplementary arginine vasopressin (AVP) infusion is increasingly being used to stabilize cardiocirculatory function in patients with advanced vasodilatory shock. However, the exact mechanism responsible for the vasopressin deficiency remains to be determined. Here we show that high mobility group box 1 protein (HMGB1), a late mediator of endotoxin lethality, is responsible for the vasopressin deficiency in endotoxemic rats. Administration of a neutralizing antibody against HMGB1 increased plasma vasopressin levels in endotoxemic rats, while administration of exogenous HMGB1 decreased plasma vasopressin levels.

Free Research Field

血栓症