Circulatory Failure During Noninhaled Forms of Cyanide Intoxication.
Circulatory Failure During Noninhaled Forms of Cyanide Intoxication.
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DOI：
10.1097/shk.0000000000000732
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发表时间：
2017-03
期刊：
影响因子：
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通讯作者：
Sonobe T
中科院分区：
文献类型：
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作者：
Haouzi P;Tubbs N;Rannals MD;Judenherc-Haouzi A;Cabell LA;McDonough JA;Sonobe T
我们的目的是确定如何循环衰竭发展后，全身施用氰化钾（KCN）。我们采用非吸入中毒方式，其中呼吸方式的改变不会影响CN在血液中的扩散，类似于摄入有毒水平的CN的影响。在一组300-400 g的大鼠中，CN诱导的昏迷（CN IP, 7 mg/kg）在2-3分钟内产生中心性呼吸暂停，并伴有强效和长时间的喘息模式，导致38%的动物自动复苏。然而，在存活的动物中观察到运动障碍和神经元坏死。为了阐明导致潜在的自动复苏与心脏骤停的机制，12只麻醉的大鼠在7-8分钟内暴露于可能导致呼吸抑制的最低水平的CN中；该剂量平均为0.375 mg/kg/min iv。在此中毒水平下，仅在呼吸暂停发作后几分钟出现心脏抑制，当PaO2达到15 Torr左右时导致心脏骤停，除非通过机械通气或自发喘气维持呼吸。在10只动物中，较高水平的KCN暴露引发了原发性心脏抑制，尽管机械通气维持了PaO2，但无脉电活动导致心脏快速骤停。这些影响与KCN中所含钾完全无关。结论是，循环衰竭可发展为CN诱导的呼吸暂停的直接后果，但在狭窄的暴露范围内。在这个“低”范围内，暴露后通过机械通气（或自发呼吸）维持肺气体交换可以逆转心脏抑制并恢复自发呼吸。在较高水平的中毒情况下，心脏抑制被视为CN暴露的一种特定的、自发不可逆的后果，导致无脉电活动。
Our objective was to determine how circulatory failure develops following systemic administration of potassium cyanide (KCN). We used a non-inhaled modality of intoxication, wherein the change in breathing pattern would not influence the diffusion of CN into the blood, akin to the effects of ingesting toxic levels of CN. In a group of 300–400 g rats, CN-induced coma (CN IP, 7 mg/kg) produced a central apnea within 2–3 minutes along with a potent and prolonged gasping pattern leading to auto-resuscitation in 38% of the animals. Motor deficits and neuronal necrosis were nevertheless observed in the surviving animals. To clarify the mechanisms leading to potential auto-resuscitation versus asystole, 12 urethane-anesthetized rats were then exposed to the lowest possible levels of CN exposure that would lead to breathing depression within 7–8 minutes; this dose averaged 0.375 mg/kg/min iv. At this level of intoxication, a cardiac depression developed several minutes only after the onset of the apnea, leading to cardiac asystole as PaO2 reached value around 15 Torr, unless breathing was maintained by mechanical ventilation or through spontaneous gasping. Higher levels of KCN exposure in 10 animals provoked a primary cardiac depression, which led to a rapid cardiac arrest by pulseless electrical activity despite the maintenance of PaO2 by mechanical ventilation. These effects were totally unrelated to the potassium contained in KCN. It is concluded that circulatory failure can develop as a direct consequence of CN induced apnea but in a narrow range of exposure. In this “low” range, maintaining pulmonary gas exchange after exposure, through mechanical ventilation (or spontaneous gasping) can reverse cardiac depression and restore spontaneous breathing. At higher level of intoxication, cardiac depression is to be treated as a specific and spontaneously irreversible consequence of CN exposure, leading to a pulseless electrical activity.