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Experimental Studies on Death by Fire in Automobiles and Exhaust Gas Poisoning

 

作者: Sanae Takeichi,   Itsuo Tokunaga,   Michihiko Maeiwa,   Kazaru Okada,   Keizo Kanbara,   Hidetoshi Nii,   Kazuyoshi Nanishi,   Takeshi Oka,  

 

期刊: The American Journal of Forensic Medicine and Pathology  (OVID Available online 1986)
卷期: Volume 7, issue 4  

页码: 301-304

 

ISSN:0195-7910

 

年代: 1986

 

出版商: OVID

 

关键词: Automobiles;Fire;Exhaust gas;Carboxyhemoglobin;Cyanide;Blood gases

 

数据来源: OVID

 

摘要:

Studies were made on the acid-base balance, blood gases carbon monoxide (CO), cyanide sulfur dioxide concentrations in the blood of albino rabbits that died from automobile exhaust gas poisoning (group I) or fires in cares (complete combustion, group II; incomplete combustion, group III). In group I, the temperature and CO concentration increased gradually to 35°C and 5.2% in 70 min. The animals died after 9 min, when the values were 20°C and 5.2%, respectively. In group II the animals died after 9 min, when the values were 55°C and 1.95%, respectively. In group III, the temperature was very high (870°C), but the CO concentration was not (0.6–1.3%) after 4 min. The animals died after 5 min.In all experimental groups, marked acidosis and hypoxemia were seen, but the CO2tension (PCO2) was high, in contrast to previous studies on pure CO poisoning. In group I, the level of carboxyhemoglobin (CO-Hb) was significantly higher (91.2 ± 3.4% in arterial blood, 87.5 ± 8.1% in venous blood; p < 0.01) than in groups II and III. Although the O2tensions of venous and arterial blood (PvO2, PaO2) were very low, that of arterial blood was higher, suggesting that O2was still being utilized in the tissues at the time of death. In group II, CO-Hb was high (57.7 ± 16.0% in arterial blood, 61.2 ± 20.6% in venous blood) and the acid-base balance indicated marked acidosis. In group III, the CO-Hb, Pco2and cyanide levels in the blood were very high. CO and CO2might be produced by either type of combustion cyanide by a pyrolytic reaction of nitrogenous material. The high Pco2value suggested respiratory acidosis induced by inhibition of the central respiratory center by CO and/or cyanide. PaO2and PvO2were similar, suggesting that intracellular respiration was blocked by cyanide, the level of which was significantly higher than in group II (p < 0.01). Sulfur dioxide was not detected in any of the groups.It is concluded that in group II and more especially group I, CO may be the main lethal factor and that marked acidosis was induced by asphyxiation owing to CO and deficient O2. In group III, the primary cause of death may have been CO poisoning, with consequent inhibition of the cytochrome system by cyanide and O2deficiency.

 

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