Eikermann Matthias, Fassbender Philipp, Malhotra Atul, Takahashi Masaya, Kubo Shigeto, Jordan Amy S, Gautam Shiva, White David P, Chamberlin Nancy L
Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02114-2696, USA.
Anesthesiology. 2007 Oct;107(4):621-9. doi: 10.1097/01.anes.0000281928.88997.95.
It is standard practice to administer a cholinesterase inhibitor (e.g., neostigmine) at the end of a surgical case to reverse suspected effects of neuromuscular blocking agents regardless of whether such residual effects are present. The authors hypothesized that cholinesterase inhibition when given the in absence of neuromuscular blockade (NB) would decrease upper airway dilatory muscle activity and consequently upper airway volume.
The authors measured genioglossus and diaphragm electromyograms during spontaneous ventilation in anesthetized, tracheostomized rats before and after administration of neostigmine (0.03, 0.06, or 0.12 mg/kg), after recovery of the train-of-four ratio (quadriceps femoris muscle) to unity after NB (n = 18). For comparison, the authors made the same measurements in rats that had no previous NB (n = 27). In intact anesthetized rats, the authors measured upper airway volume and end-expiratory lung volume by magnetic resonance imaging before and after 0.12 mg/kg neostigmine (n = 9).
Neostigmine treatment in rats that had fully recovered from NB based on the train-of-four ratio caused dose-dependent decreases in genioglossus electromyogram (to 70.3 +/- 7.6, 49.2 +/- 3.2, and 39.7 +/- 2.3% of control, respectively), decreases in diaphragm electromyogram (to 103.1 +/- 6.5, 83.1 +/- 4.7, and 68.7 +/- 7.3% of control), and decreases in minute ventilation to a nadir value of 79.6 +/- 6% of preneostigmine baseline. Genioglossus electromyogram effects were the same when neostigmine was given with no previous NB. Neostigmine caused a decrease in upper airway volume to 83 +/- 3% of control, whereas end-expiratory lung volume remained constant.
The cholinesterase inhibitor neostigmine markedly impairs upper airway dilator volume, genioglossus muscle function, diaphragmatic function, and breathing when given after recovery from vecuronium-induced neuromuscular block.
在手术结束时常规使用胆碱酯酶抑制剂(如新斯的明)来逆转疑似神经肌肉阻滞剂的作用,无论是否存在此类残余效应。作者推测,在不存在神经肌肉阻滞(NB)的情况下给予胆碱酯酶抑制剂会降低上气道扩张肌的活性,进而减少上气道容积。
作者在麻醉、气管切开的大鼠自主通气期间,于给予新斯的明(0.03、0.06或0.12mg/kg)之前及之后,以及在NB后四个成串刺激比值(股四头肌)恢复至1时进行测量颏舌肌和膈肌的肌电图(n = 18)。为作比较,作者在未曾接受NB的大鼠中进行相同测量(n = 27)。在完整的麻醉大鼠中,作者通过磁共振成像在给予0.12mg/kg新斯的明之前及之后测量上气道容积和呼气末肺容积(n = 9)。
根据四个成串刺激比值已从NB完全恢复的大鼠,给予新斯的明治疗导致颏舌肌肌电图呈剂量依赖性降低(分别降至对照值的70.3±7.6%、49.2±3.2%和39.7±2.3%),膈肌肌电图降低(降至对照值的103.1±6.5%、83.1±4.7%和68.7±7.3%),分钟通气量降至新斯的明给药前基线值的79.6±6%的最低点。在未曾接受NB的情况下给予新斯的明时,颏舌肌肌电图的效应相同。新斯的明使上气道容积降至对照值的83±3%,而呼气末肺容积保持不变。
从维库溴铵诱导的神经肌肉阻滞恢复后给予胆碱酯酶抑制剂新斯的明,会显著损害上气道扩张肌容积、颏舌肌功能、膈肌功能及呼吸。