Department of Anesthesiology and Pain Medicine, Inje University Seoul Paik Hospital, Seoul, Korea.
Neuromuscular Physiology Research Team at the Laboratory of Animal Research, Asan Institute of Life Science, Seoul, Korea.
Korean J Anesthesiol. 2019 Aug;72(4):366-374. doi: 10.4097/kja.d.18.00238. Epub 2019 Mar 19.
The facilitator effects of steroids on neuromuscular transmission may cause resistance to neuromuscular blocking agents. Additionally, steroids may hinder sugammadex reversal of neuromuscular blockade, but these findings remain controversial. Therefore, we explored the effect of dexamethasone and hydrocortisone on rocuronium-induced neuromuscular blockade and their inhibitory effect on sugammadex.
We explored the effects of steroids, dexamethasone and hydrocortisone, in vitro using a phrenic nerve-hemidiaphragm rat model. In the first phase, an effective dose of rocuronium was calculated, and in the second phase, following sugammadex administration, the recovery of the train-of-four (TOF) ratio and T1 was evaluated for 30 minutes, and the recovery index was calculated in dexamethasone 0, 0.5, 5, and 50 μg/ml, or hydrocortisone 0, 1, 10, or 100 μg/ml.
No significant effect of steroids on the effective dose of rocuronium was observed. The TOF ratios at 30 minutes after sugammadex administration were decreased significantly only at high experimental concentrations of steroids: dexamethasone 50 μg/ml and hydrocortisone 100 μg/ml (P < 0.001 and P = 0.042, respectively). There were no statistical significances in other concentrations. No differences were observed in T1. Recovery index was significantly different only in 100 μg/ml of hydrocortisone (P = 0.03).
Acute exposure to steroids did not resist the neuromuscular blockade caused by rocuronium. And inhibition of sugammadex reversal on rocuronium-induced neuromuscular blockade is unlikely at typical clinical doses of dexamethasone and also hydrocortisone. Conclusively, we can expect proper effects of rocuronium and sugammadex when dexamethasone or hydrocortisone is used during general anesthesia.
类固醇对神经肌肉传递的促进作用可能导致神经肌肉阻滞剂产生耐药性。此外,类固醇可能会阻碍琥珀酸舒更葡糖钠逆转神经肌肉阻滞,但这些发现仍存在争议。因此,我们探讨了地塞米松和氢化可的松对罗库溴铵诱导的神经肌肉阻滞的影响及其对琥珀酸舒更葡糖钠的抑制作用。
我们使用膈神经-膈肌大鼠模型在体外研究了类固醇(地塞米松和氢化可的松)的作用。在第一阶段,计算了罗库溴铵的有效剂量,在第二阶段,给予琥珀酸舒更葡糖钠后,评估了 30 分钟时的四成肌松比(TOF)比值和 T1 的恢复情况,并计算了地塞米松 0、0.5、5 和 50 μg/ml 或氢化可的松 0、1、10 或 100 μg/ml 时的恢复指数。
类固醇对罗库溴铵的有效剂量没有显著影响。仅在高实验浓度的类固醇时,琥珀酸舒更葡糖钠给药后 30 分钟的 TOF 比值显著降低:地塞米松 50 μg/ml 和氢化可的松 100 μg/ml(P < 0.001 和 P = 0.042)。在其他浓度下没有统计学意义。T1 没有差异。仅在氢化可的松 100 μg/ml 时,恢复指数有显著差异(P = 0.03)。
急性暴露于类固醇不会抵抗罗库溴铵引起的神经肌肉阻滞。并且在典型的临床剂量的地塞米松和氢化可的松下,琥珀酸舒更葡糖钠逆转罗库溴铵诱导的神经肌肉阻滞的抑制作用不太可能。综上所述,当全身麻醉时使用地塞米松或氢化可的松时,可以预期罗库溴铵和琥珀酸舒更葡糖钠的效果。