The establishment of a control system for HIF1alpha activation pathway in post-cardiac arrest syndrome.

2014 Fiscal Year Final Research Report

• Project/Area Number: 25861736
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Emergency medicine
• Research Institution: Hokkaido University
• Principal Investigator: WADA TAKESHI 北海道大学, 大学病院, 助教 (30455646)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: 生体侵襲 / 臓器不全 / 凝固線溶系 / VEGF / Angiopoietin

Outline of Final Research Achievements

I investigated the important role of fibrinolysis which are involved in neutrophil elastase and plasmin, which is affected by plasminogen activator inhibitor-1 (PAI-1), which is induced by Hypoxia inducible factor-1α (HIF1α) in post-cardiac arrest syndrome (PCAS). The results indicated that fibrinolytic shutdown plays important roles in the development of organ dysfunction in PCAS patients. Neutrophil elastase-mediated fibrinolysis cannot overcome the fibrinolytic shutdown that occurs in DIC patients with PCAS, thus resulting in the development of multiple organ dysfunction.
In addition, I studied the relationship between the serum levels of HIF1α and the development of DIC or organ dysfunction in sepsis, severe trauma, and PCAS patients. These studies showed no significant results. This can be explained by the fact that HIF1α acts inside the cell.

Free Research Field

医歯薬学