2-甲氧基-3,5-二硝基苯胺 | 114168-47-7

• 分子结构分类: 有机化合物 - 苯类化合物 - 苯和取代衍生物
• 中文名称: 2-甲氧基-3,5-二硝基苯胺
• 英文名称: 2-methoxy-3,5-dinitro-aniline
• 英文别名: 4.6-Dinitro-2-amino-phenol-methylaether；2-Methoxy-3,5-dinitro-anilin；4.6-Dinitro-2-amino-anisol；2-Methoxy-3,5-dinitroaniline
• CAS: 114168-47-7
• 化学式: C₇H₇N₃O₅
• 分子量: 213.15
• InChiKey: SZBYMOUYGPKBTO-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  0.7
• 重原子数：
  15
• 可旋转键数：
  1
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.14
• 拓扑面积：
  127
• 氢给体数：
  1
• 氢受体数：
  6

反应信息

• 作为产物：
  描述：

  2,4,6-三硝基苯甲醚 在 ammonium sulfide 作用下， 生成 2-甲氧基-3,5-二硝基苯胺
  参考文献：
  名称：

  Adrenocortical Dysfunction Following Etomidate Induction in Emergency Department Patients

  摘要：

  Abstract. Objective: To assess adrenocortical function following intravenous etomidate use in emergency department (ED) patients requiring intubation. Methods: This was a prospective, randomized, controlled trial of consecutive patients presenting to the ED requiring intubation. Patients were randomized to receive a single bolus induction dose of either 0.05‐0.1 mg/kg midazolam (control group) or 0.3 mg/kg etomidate (etomidate group) during a standardized rapid‐sequence intubation (RSI) with succinylcholine. The primary outcome variable was adrenocortical function at 4, 12, and 24 hours post‐induction as assessed by measured serum cortisol response to exogenous cosyntropin (cosyntropin stimulation test, CST). Fisher's exact test was used to compare CST results between groups. Results: Thirty‐one patients were enrolled: 8 control, 10 etomidate, and 13 excluded from analysis for either incomplete data or steroid use during the study period. The 4‐hour CST results were significantly different between study groups, with a normal response in 100% of control patients vs 30% of etomidate patients (p = 0.004). The 12‐ and 24‐hour CSTs did not differ significantly between groups: normal CST in 100% of control patients at 12 and 24 hours vs 100% and 90% among etomidate patients at 12 and 24 hours, respectively (p = 1.0 at 12 and 24 hours). Measured cortisol levels of patients with abnormal CSTs remained within normal laboratory reference ranges. Conclusion: Use of etomidate in ED patients requiring RSI results in adrenocortical dysfunction. However, cortisol levels remain within normal laboratory levels during this period of dysfunction. Adrenocortical dysfunction appears to resolve within 12 hours of a single bolus dose of 0.3 mg/kg etomidate.

  DOI：

  10.1111/j.1553-2712.2001.tb00537.x

文献信息

• BILKIS I. I.; USKOV S. I.; SHTEJNGARTS V. D., IZV. CO AN CCCP. CEP. XIM. N.,(1987) N 9/3, 111-121
  作者：BILKIS I. I.、 USKOV S. I.、 SHTEJNGARTS V. D.

  DOI：——

  日期：——
• Adrenocortical Dysfunction Following Etomidate Induction in Emergency Department Patients
  作者：Christina L. Schenarts、John H. Burton、Richard R. Riker

  DOI：10.1111/j.1553-2712.2001.tb00537.x

  日期：2001.1

  Abstract. Objective: To assess adrenocortical function following intravenous etomidate use in emergency department (ED) patients requiring intubation. Methods: This was a prospective, randomized, controlled trial of consecutive patients presenting to the ED requiring intubation. Patients were randomized to receive a single bolus induction dose of either 0.05‐0.1 mg/kg midazolam (control group) or 0.3 mg/kg etomidate (etomidate group) during a standardized rapid‐sequence intubation (RSI) with succinylcholine. The primary outcome variable was adrenocortical function at 4, 12, and 24 hours post‐induction as assessed by measured serum cortisol response to exogenous cosyntropin (cosyntropin stimulation test, CST). Fisher's exact test was used to compare CST results between groups. Results: Thirty‐one patients were enrolled: 8 control, 10 etomidate, and 13 excluded from analysis for either incomplete data or steroid use during the study period. The 4‐hour CST results were significantly different between study groups, with a normal response in 100% of control patients vs 30% of etomidate patients (p = 0.004). The 12‐ and 24‐hour CSTs did not differ significantly between groups: normal CST in 100% of control patients at 12 and 24 hours vs 100% and 90% among etomidate patients at 12 and 24 hours, respectively (p = 1.0 at 12 and 24 hours). Measured cortisol levels of patients with abnormal CSTs remained within normal laboratory reference ranges. Conclusion: Use of etomidate in ED patients requiring RSI results in adrenocortical dysfunction. However, cortisol levels remain within normal laboratory levels during this period of dysfunction. Adrenocortical dysfunction appears to resolve within 12 hours of a single bolus dose of 0.3 mg/kg etomidate.