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气态物质导致的缺氧性窒息。

Asphyxia due to oxygen deficiency by gaseous substances.

作者信息

Watanabe T, Morita M

机构信息

Department of Legal Medicine, School of Medicine, Sapporo Medical University, School of Medicine, Japan.

出版信息

Forensic Sci Int. 1998 Aug 31;96(1):47-59. doi: 10.1016/s0379-0738(98)00112-1.

Abstract

The determination of the cause of death in asphyxiation gas cases is very difficult because of the variation in circumstances surrounding such deaths. To clarify the cause of death and to identify the factors involved in asphyxia, the symptoms during asphyxia, the concentration of gases at the respiratory arrest, the time to death and the concentration of the gaseous substances in the tissues were studied using rats and six gases. Three inhalations were used: (1) rapid asphyxia (2-3 min) in the exposure chamber in which the oxygen was depleted completely, (2) prolonged asphyxia (20-25 min) by gradually depleted oxygen, and (3) asphyxia by the inhalation of gases saturated with a critical gas concentration, maintaining the O2 at 20% (60 min). In the rapid asphyxia groups, respiratory arrest occurred within 30 to 40 s, followed by cardiac arrest 2 or 3 min thereafter. Severe convulsions were observed only with the use of nitrogen. In the prolonged asphyxia groups, respiratory arrest occurred at the concentration of 4-5% O2 with non-toxic gases (N2, CH4, N2O, and propane). The toxic gases CO2 and Freon-22 produced respiratory arrest at the concentration of 6.6-8.0% O2 (60-67% CO2) and 13-14% of O2 (30-35% Freon-22), respectively. Variations in the concentrations of the gases among the tissues was observed according to the type of asphyxia, type of gas and the duration of exposure. The concentration of the fat-soluble gases in the adipose tissue showed marked variation according to the duration of the exposure. The distribution pattern of methane was different from those of the other gases, in which the variation of concentrations among the tissues except lung were little in both rapid and prolonged asphyxia. These phenomena were considered to be attributable to the solubility of the gaseous substances in blood and tissues. Atrophy in the alveoli was observed after the rapid asphyxia with CO2 and N2O. Local hemorrhaging in the lungs was also observed, especially in CO2 asphyxia. The risks of oxygen-depletion asphyxia are the rapid reaction of loss of consciousness and respiratory and cardiac arrest. This paper presents valuable findings for the diagnosis of the cause of death and estimating the situation of the accident in cases of asphyxia.

摘要

由于窒息性气体中毒死亡案件的相关情况各不相同,因此确定其死因非常困难。为了明确死因并找出与窒息相关的因素,我们使用大鼠和六种气体,对窒息过程中的症状、呼吸停止时的气体浓度、死亡时间以及组织中气态物质的浓度进行了研究。采用了三种吸入方式:(1)在氧气完全耗尽的暴露舱中快速窒息(2 - 3分钟);(2)通过逐渐耗尽氧气进行长时间窒息(20 - 25分钟);(3)吸入临界气体浓度饱和的气体,同时将氧气维持在20%(60分钟)进行窒息。在快速窒息组中,呼吸在30至40秒内停止,随后在2或3分钟后心脏停止跳动。仅在使用氮气时观察到严重抽搐。在长时间窒息组中,对于无毒气体(氮气、甲烷、一氧化二氮和丙烷),呼吸在氧气浓度为4 - 5%时停止。有毒气体二氧化碳和氟利昂 - 22分别在氧气浓度为6.6 - 8.0%(二氧化碳浓度为60 - 67%)和13 - 14%(氟利昂 - 22浓度为30 - 35%)时导致呼吸停止。根据窒息类型、气体类型和暴露持续时间的不同,观察到组织间气体浓度存在差异。脂肪组织中脂溶性气体的浓度根据暴露持续时间有显著变化。甲烷的分布模式与其他气体不同,在快速和长时间窒息中,除肺部外的其他组织中其浓度变化很小。这些现象被认为归因于气态物质在血液和组织中的溶解度。在二氧化碳和一氧化二氮快速窒息后观察到肺泡萎缩。肺部还出现局部出血,尤其是在二氧化碳窒息时。缺氧窒息的风险是意识丧失、呼吸和心脏骤停的快速反应。本文为窒息案件的死因诊断和事故情况评估提供了有价值的发现。

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