Vick J A, Von Bredow J D
Division of Research and Testing, Food and Drug Administration, Washington, DC 20204, USA.
J Appl Toxicol. 1996 Nov-Dec;16(6):509-16. doi: 10.1002/(SICI)1099-1263(199611)16:6<509::AID-JAT382>3.0.CO;2-V.
Successful first aid therapy for cyanide intoxication is dependent upon immediate administration of antidotes which directly or indirectly interact with the cyanide ion to remove it from circulation. Owing to the severe respiratory, cardiovascular and convulsive episodes following acute cyanide intoxication, the most practical approach is to administer antidotes by intramuscular injection. Exceptionally rapid methemoglobin formers-hydroxylamine hydrochloride (HH) and dimethylaminophenol (DMAP)-are usually able to prevent the lethal effect of cyanide following intramuscular injections in doses sufficient to induce 20% methemoglobin (HH = 20 mg kg-1 and DMAP = 2 mg kg-1). Sodium nitrite, the methemoglobin inducer approved for military use, must be administered by intravenous infusion because it is not an effective cyanide antidote by the intramuscular route. In the normal unintoxicated animal an intramuscular injection of 20 mg kg-1 sodium nitrite will form 20% methemoglobin; however, in acute cyanide intoxication the associated severe bradycardia appears to limit the rate of absorption and thus the rapid formation of methemoglobin. If the bradycardia is prevented or reversed by atropine, the rate of absorption of sodium nitrite and the formation of methemoglobin is able to reverse the otherwise lethal effects of cyanide. Thus, an intramuscularly administered combination of 20 mg kg-1 sodium nitrite and 1 mg kg-1 atropine sulfate, rapidly absorbed from the intramuscular site, appears to achieve the same degree of effectiveness against acute cyanide intoxication as intramuscularly administered HH or DMAP. It would appear from these studies that HH, DMAP and sodium nitrite with atropine are all potentially effective intramuscular antidotes for acute cyanide poisoning.
氰化物中毒的成功急救治疗取决于立即给予解毒剂，这些解毒剂直接或间接与氰离子相互作用，将其从循环中清除。由于急性氰化物中毒后会出现严重的呼吸、心血管和惊厥发作，最实际的方法是通过肌肉注射给予解毒剂。异常快速的高铁血红蛋白形成剂——盐酸羟胺（HH）和二甲氨基苯酚（DMAP）——通常能够在肌肉注射足以诱导20%高铁血红蛋白的剂量（HH = 20 mg/kg和DMAP = 2 mg/kg）后预防氰化物的致死作用。亚硝酸钠是被批准用于军事用途的高铁血红蛋白诱导剂，必须通过静脉输注给药，因为它通过肌肉注射途径不是一种有效的氰化物解毒剂。在正常未中毒的动物中，肌肉注射20 mg/kg的亚硝酸钠会形成20%的高铁血红蛋白；然而，在急性氰化物中毒时，相关的严重心动过缓似乎会限制吸收速度，从而限制高铁血红蛋白的快速形成。如果通过阿托品预防或逆转心动过缓，亚硝酸钠的吸收速度和高铁血红蛋白的形成能够逆转氰化物原本的致死作用。因此，肌肉注射20 mg/kg的亚硝酸钠和1 mg/kg的硫酸阿托品的组合，从肌肉部位快速吸收，似乎在对抗急性氰化物中毒方面能达到与肌肉注射HH或DMAP相同程度的有效性。从这些研究来看，HH、DMAP以及亚硝酸钠与阿托品都是急性氰化物中毒潜在有效的肌肉注射解毒剂。
