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Study for the induction mechanism of the shock-Investigation on the burn shock model-

Research Project

Project/Area Number 17590590
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Legal medicine
Research InstitutionUniversity of Occupational and Environmental Health

Principal Investigator

KITA Toshiro  University of Occupational and Environmental Health, School of Medicine, Associate Professor, 医学部, 助教授 (00131912)

Co-Investigator(Kenkyū-buntansha) TANAKA Toshiko  University of Occupational and Environmental Health, School of Medicine, Assistant Professor, 医学部, 講師 (80141745)
Project Period (FY) 2005 – 2006
Project Status Completed (Fiscal Year 2006)
Budget Amount *help
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2006: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2005: ¥2,000,000 (Direct Cost: ¥2,000,000)
KeywordsShock / Cause of death / Marker / Polymorphonuclear leukocytes / Apoptosis / Burn / p38MAPK / Cytokine / 心臓 / 臓器障害 / MAPK / サイトカイン
Research Abstract

We approached to the induction mechanism of shock, and we investigated what etiology induced these morphological changes after shock in order to identify shock as the cause of death. The aim of this experiment sought to explain the cause of cardiac dysfunction following burn shock and search a marker of shock. So, we investigated the induction of inflammatory cells (PMNs), apoptosis and Hsp70 of the myocardial tissue as a marker of shock. Added to this, we approached the role of p38MAPK on the cardiac failure after burn injury using a specific inhibitor of p38MAPK (FR167653).
At 2 hours after burn, we observed the induction of p38MAPK and myocardial apoptosis after burn injury using infant rat model. Subsequently, activation of cytokine (TNF-α) and the appearance of inflammatory cells (PMNs) are observed at 6 hours after burn. The inductions of Hsp70 in the myocardial tissue after burn are not clearly observed. FR167653 prevented the activation of p38MAPK in the heart and, finally, prevented burn-induced heart failure. So we identified the pathophysiologic role of the p38MAPK pathway in the development of heart failure after burn.
Forensic practice
Our experimental burn shock data showed the induction of apoptosis and PMNs after burn injury. Consequently, we used the apoptosis and PMNs staining method, and we immunohistochemically investigated several organs of our practical autopsy cases to detect the appearance of apoptosis and PMNs as a marker of shock induction. We compared the hemorrhagic shock with other causes of death, such as blood loss, asphyxia, drawing and head injury. In every organ, a significant induction of apoptosis and PMNs were observed in the hemorrhagic shock compared to the other causes of death.
Therefore, detecting the induction of apoptosis and PMNs as a marker of shock is a very useful and significant method for judging the cause of death in forensic practice.

Report

(3 results)
  • 2006 Annual Research Report   Final Research Report Summary
  • 2005 Annual Research Report

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Published: 2005-04-01   Modified: 2016-04-21  

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