Yanagisawa N, Morita H, Nakajima T
Kanto Rosai Hospital, 1-1, Kizukisumiyoshicho, Nakahara-ku, Kawasaki, 211-8510, Japan.
J Neurol Sci. 2006 Nov 1;249(1):76-85. doi: 10.1016/j.jns.2006.06.007. Epub 2006 Sep 7.
Two terrorist attacks with the nerve agent Sarin affected citizens in Matsumoto and Tokyo, Japan in 1994 and 1995, killing 19 and injuring more the 6000. Sarin, a very potent organophosphate nerve agent, inhibits acetylcholinesterase (AchE) activity within the central, peripheral, and autonomic nervous systems. Acute and long-term Sarin effects upon humans were well documented in these two events. Sarin gas inhalation caused instantaneous death by respiratory arrest in 4 victims in Matsumoto. In Tokyo, two died in station yards and another ten victims died in hospitals within a few hours to 3 months after poisoning. Six victims with serum ChE below 20% of the lowest normal were resuscitated from cardiopulmonary arrest (CPA) or coma with generalized convulsion. Five recovered completely and one remained in vegetative state due to anoxic brain damage. EEG abnormalities persisted for up to 5 years. Miosis and copious secretions from the respiratory and GI tracts (muscarinic effects) were common in severely to slightly affected victims. Weakness and twitches of muscles (nicotinic effects) appeared in severely affected victims. Neuropathy and ataxia were observed in small number (less than 10%) of victims, which findings disappeared between 3 days and 3 months. Leukocytosis and high serum CK levels were common. Hyperglycemia, ketonuria, low serum triglyceride, hypopotassemia were observed in severely affected victims, which abnormalities were attributed to damage of the adrenal medulla. Oximes, atropine sulphate, diazepam and ample intravenous infusion were effective treatments. Pralidoxime iodide IV reversed cholinesterase and symptoms quickly even if administered 6 h after exposure. Post Traumatic Stress Disorder (PTSD) was less than 8% after 5 years. However, psychological symptoms continue in victims of both incidents. In summary, both potent toxicity and quick recovery from critical ill conditions were prominent features. Conventional therapies proved effective in Sarin incidents in Japan.
1994年和1995年，日本松本和东京发生了两起使用神经性毒剂沙林的恐怖袭击事件，造成19人死亡，6000多人受伤。沙林是一种毒性极强的有机磷神经毒剂，可抑制中枢、外周和自主神经系统内的乙酰胆碱酯酶（AchE）活性。这两起事件对人类的急性和长期影响都有详细记录。在松本，4名受害者因吸入沙林毒气，呼吸骤停，当场死亡。在东京，有两人在车站广场死亡，另有10名受害者在中毒后数小时至3个月内死亡。6名血清胆碱酯酶低于正常最低值20%的受害者，从心肺骤停（CPA）或伴有全身抽搐的昏迷中复苏。5人完全康复，1人因缺氧性脑损伤而处于植物人状态。脑电图异常持续了5年。瞳孔缩小以及呼吸道和胃肠道大量分泌物（毒蕈碱样作用）在重度至轻度中毒受害者中很常见。重度中毒受害者出现肌肉无力和抽搐（烟碱样作用）。少数（不到10%）受害者出现神经病变和共济失调，这些症状在3天至3个月内消失。白细胞增多和血清肌酸激酶水平升高很常见。重度中毒受害者出现高血糖、酮尿、血清甘油三酯降低、低钾血症，这些异常归因于肾上腺髓质损伤。肟类、硫酸阿托品、地西泮和大量静脉输液是有效的治疗方法。即使在接触后6小时给药，静脉注射碘解磷定也能迅速逆转胆碱酯酶抑制并缓解症状。5年后创伤后应激障碍（PTSD）发生率低于8%。然而，两起事件的受害者都持续存在心理症状。总之，毒性强和从危重症中快速恢复是显著特征。在日本的沙林事件中，传统疗法被证明是有效的。
