Department of Legal Medicine, Osaka City University Medical School, Asahi-machi 1-4-3, Abeno, Osaka, 545-8585, Japan.
Int J Legal Med. 2012 Jul;126(4):581-7. doi: 10.1007/s00414-012-0698-2. Epub 2012 May 3.
Drowning involves complex fatal factors, including asphyxiation and electrolyte/osmotic disturbances, as well as hypothermia in cold water. The present study investigated the molecular pathology of pulmonary injury due to drowning, using lung specimens from forensic autopsy cases of drowning (n = 21), acute mechanical asphyxia due to neck compression and smothering (n = 24), and hypothermia (cold exposure, n = 11), as well as those of injury (n = 23), intoxication (n = 13), fire fatality (n = 18), and acute cardiac death (n = 9) for comparison. TaqMan real-time reverse transcription polymerase chain reaction was used to quantify messenger RNA (mRNA) expressions of pulmonary surfactant-associated proteins A and D (SP-A and SP-D), tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-10. SP-A and SP-D mRNA levels were lower for drowning, mechanical asphyxiation, fire fatality, and acute cardiac deaths than for hypothermia and injury. TNF-α, IL-1β, and IL-10 mRNA levels were higher for drowning or for drowning and injury than for other groups; there was no significant difference between fire fatality, involving airway injury due to inhalation of hot/irritant gases, and other control groups. These observations suggest characteristic molecular biological patterns of pulmonary injury involving suppression of pulmonary surfactants and activation of early-phase mediators of inflammation in drowning, with high mRNA expression levels of pulmonary surfactants in fatal hypothermia; however, there was no significant difference among these markers in immunohistochemical detection, except for SP-A. These mRNA expressions can be used as markers of pulmonary injury to assist in investigations of the pathophysiology of drowning and fatal hypothermia in combination with other biochemical and biological markers.
溺水涉及复杂的致死因素,包括窒息和电解质/渗透紊乱,以及冷水导致的体温过低。本研究通过法医尸检溺水(n=21)、颈部压迫和捂压导致的急性机械性窒息(n=24)、低温(寒冷暴露,n=11)、损伤(n=23)、中毒(n=13)、火灾死亡(n=18)和急性心脏死亡(n=9)的肺损伤案例的肺组织标本,研究了溺水导致的肺损伤的分子病理学。采用 TaqMan 实时逆转录聚合酶链反应定量分析肺表面活性物质相关蛋白 A 和 D(SP-A 和 SP-D)、肿瘤坏死因子(TNF)-α、白细胞介素(IL)-1β 和 IL-10 的信使 RNA(mRNA)表达。与低温和损伤相比,溺水、机械性窒息、火灾死亡和急性心脏死亡的 SP-A 和 SP-D mRNA 水平较低。与其他组相比,溺水或溺水和损伤组的 TNF-α、IL-1β 和 IL-10 mRNA 水平较高;涉及吸入热/刺激性气体导致气道损伤的火灾死亡与其他对照组之间没有显著差异。这些观察结果表明,溺水涉及肺表面活性剂抑制和炎症早期介质激活,具有致命性低温时肺表面活性剂高 mRNA 表达的特征性分子生物学肺损伤模式;但是,除了 SP-A 之外,这些标志物在免疫组织化学检测中没有显著差异。这些 mRNA 表达可作为肺损伤的标志物,与其他生化和生物标志物结合使用,有助于研究溺水和致命性低温的病理生理学。