Control mechanisms and its failure of endothelial hyperpermeability in sepsis: from a view point of erythrocyte and platelet

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K11000
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Emergency medicine
• Research Institution: Kurume University
• Principal Investigator: Takasu Osamu 久留米大学, 医学部, 教授 (90236216)
• Co-Investigator(Kenkyū-buntansha): 新山 修平 久留米大学, 医学部, 准教授 (40258455)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 敗血症 / 臓器不全 / 血管透過性亢進

Outline of Final Research Achievements

Endothelial hyper permeability is attracted attention as one of the mechanisms of the organ failure in critically ill patients. The purpose of this study was to clarify the potential of platelets or erythrocytes as modulator of the endothelial hyperpermeability.
On the cecal ligation and puncture (CLP) model of mice, there was a positive correlation between the sVE-Cadherin and the extracellular water ratio (ECW% ratio) measured by bioimpedance analysis. The characteristic changes of platelets were prominent than that of erythrocytes in early phase of sepsis. Angiopoietin-1, which acts as a positive regulating factor for VE-cadherin, decreased depending the number of platelets. Administration of the platelet rich plasma (PRP) extraction containing abundant Ang-1 suppressed increase in the ECW% on CLP mice. These findings suggested that a therapeutic potential of PRP extraction for endothelial hyperpermeability.

Free Research Field

救急集中治療