Study on the mechanisms of pathogenesis of critical illness polyneuropathy and protective effect of activated factor X.

• Project/Area Number: 23592687
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Emergency medicine
• Research Institution: St. Marianna University School of Medicine
• Principal Investigator: HINO Hirofumi 聖マリアンナ医科大学, 医学部, 准教授 (70308500)
• Project Period (FY): 2011 – 2013
• Project Status: Completed (Fiscal Year 2013)
• Budget Amount: ¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000); Fiscal Year 2013: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000); Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000); Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
• Keywords: 敗血症 / 重症末梢神経炎 / 電位依存性Naチャネルサブタイプ / チャネロパチー / 末梢神経炎 / ナトリウムチャネル / glycocalyx / ダナパロイド / アンチトロンビン / 抗凝固薬

Research Abstract

We measured the expression of eight kinds of voltage-dependent sodium channel receptor subtypes (Nav) of the sciatic nerve by the real-time PCR method in sepsis induced critical illness polyneuropathy rat model (L-group) and compared to the control group (C-group). We achieved the results shown the significant reductions of gene expression in three subtypes of Nav and increases in three different kinds of Nav in L-group compared to C-group. These data implied the different types of sodium channel gene expression plays an important role in the mechanisms of pathogenesis of critical illness polyneuropathy as channelopathy.
Since the administration of Drug-X and/or Drug-Y did not improve the alteration in Nav gene expression, other actions of Drug-X and Drug-Y might be involved in the improvement of nerve function during sepsis.