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• W2328403855 abstract "Introduction: Cyanide (CN) has the potential for being used in biological war-fare. The resulting mass casualties would require treatment with an effective antidote that would be immediately available in large quantities that could be easily administered, effective, not require special storing directions, retaining potency when stored at a wide range of temperatures for long periods of time. Methods: After approval by IACUC, New-Zealand white rabbits (3-5 kg) were anesthetized by an infusion of ketamine. We monitored EKG, pulse oximetry, ETCO2, tissue oxygen, BP, RR and core temperature. Sodium cyanide (NaCN) was administered at an infusion rate of 2.2 mg/kg/hr in all rabbits until significant lactic acidosis, hypopnea and hypotension occurred. At peak CN toxicity, one group of 10 rabbits (Group A) received Sulfanegen deanol (117mg/kg) intramuscularly. This antidote administered was stored for 4 months after preparation at room temperature. The second group of 10 rabbits (Group P) received normal saline as placebo. Data are reported as mean ± SD. Significance (p<0.05) was determined by ANOVA and Fischer's exact test. Results: NaCN infusion increased CN levels (0.04 ± 0.01 to 3.99 ± 1.25 mg/L; p<0.0001) and the serum lactate levels (1 ± 0.4 to 14.8 ± 0.4 mmol/L; p<0.0001) in all rabbits. The pH decreased from 7.41 ± 0.03 to 7.14 ± 0.08, p<0.0001. After antidote 3MCP, nine rabbits in Group A survived with CN levels decreasing to 0.27 ± 0.09 mg/L, p<0.001; lactate levels decreasing to 1.9 ± 1.2 mmol/L, p<0.001 and pH levels increasing to 7.35 ± 0.03, p<0.001. All the rabbits in Group P died (p<0.0001 vs Group A) with final values of CN and lactate levels higher (CN: 5.69 ± 1.2 mg/L, p<0.0001; lactate: 15 ± 0.1 mmol/L, p<0.0001) & pH levels significantly lower (6.90 ± 0.07; p<0.0001) versus the animals that received the antidote. The results were not different when compared to those obtained with freshly prepared antidote. Conclusions: Sulfanegen Deanol stored for four months and administered intramuscularly is still effective in reversing acutely induced lethal CN toxicity. Acknowledgement: Supported by Grant NIH NINDS/5U01- NS058087" @default.
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• W2328403855 date "2013-12-01" @default.
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• W2328403855 doi "https://doi.org/10.1097/01.ccm.0000440195.00407.3d" @default.
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