Authors: Qi Wang Takaki Ishikawa Tomomi Michiue BaoLi Zhu DaWei Guan Hitoshi Maeda
Publish Date: 2012/08/11
Volume: 126, Issue: 6, Pages: 875-882
Abstract
The lung is vulnerable to trauma pulmonary edema starts quickly as part of the systemic responses involved in shock The present study investigated the molecular pathology of posttraumatic alveolar damage and responses involving pulmonary edema in forensic autopsy cases of injury n = 66 compared with acute cardiac death cases n = 13 Intrapulmonary mRNA and immunohistochemical expressions of matrix metalloproteinases MMPs MMP2 and MMP9 intercellular adhesion molecule1 claudin5 and aquaporins AQPs AQP1 and AQP5 were examined Subacute injury deaths showed an increase in lung weight similar to that in acute cardiac death but relative mRNA quantification using the Taqman realtime PCR assay demonstrated different findings among the causes of death higher expressions were detected for all markers except for AQP5 in sharp instrument injury for MMP2 in blunt brain injury and for MMP9 in nonbrain blunt injury but these expression levels were lower in acute cardiac death In immunostaining only MMPs showed differences among the causes of death MMP2 expression was evident in most subacute deaths due to blunt brain injury and sharp instrument injury whereas MMP9 was intensely positive in those of nonbrain blunt injury and sharp instrument injury These findings suggest significant differences in the mechanism of pulmonary edema among fatal injuries and acute cardiac death especially between blunt and sharp instrument injury Systematic analysis of gene expressions using realtime PCR in combination with immunohistochemistry may be useful in evaluating pulmonary damage and responses after injury in death investigations especially in connection with posttraumatic shock
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