最小神经肌肉阻滞逆转后急性低氧通气反应的恢复：一项健康非肥胖志愿者的随机对照试验
贵州医科大学 麻醉与心脏电生理课题组
翻译：周倩 编辑：周倩 审校：曹莹
神经肌肉阻滞剂会抑制外周化学反射。本研究比较了2 mg/kg和4 mg/kg舒更葡糖（sugammadex）与自然恢复对最小神经肌肉阻滞后急性低氧通气反应（AHVR）恢复的影响。
方法
这是一项在健康志愿者中开展的两实验随机对照试验。受试者通过持续输注罗库溴铵，使头颈部神经肌肉阻滞症状稳定（即症状性神经肌肉阻滞）。在第一项实验中，神经肌肉阻滞允许自然恢复；而在第二项实验中，受试者被随机分配接受2mg/Kg或4mg/Kg的舒更葡糖进行逆转治疗。通过拇指内收肌肌电图评估神经肌肉阻滞深度，并在基线、神经肌肉阻滞稳定期以及恢复后0、20和40分钟测量肌酸激酶活性（AHVR）。
结果
本研究共招募37名志愿者，其中27人的数据符合分析要求。在症状性神经肌肉阻滞期间，AHVR降低了32%（平均差异-0.22 L·%⁻¹·min⁻¹；95%置信区间为-0.32至-0.12）。当所有症状完全消失后，AHVR仍平均保持23%的抑制状态（平均差异为-0.16L·%⁻¹·min⁻¹，95%置信区间-0.28至-0.04）。数据显示，57%的志愿者在自发恢复后，其AHVR未恢复至基线水平，而接受舒更葡糖逆转治疗的志愿者中这一比例为28%。值得注意的是，与舒更葡糖逆转治疗相比，自发恢复后AHVR的抑制幅度更为显著。但所有组别在恢复后20分钟和40分钟时，AHVR均未出现与基线值有统计学差异的情况。
用舒更葡糖逆转最小神经肌肉阻滞后的AHVR与神经肌肉阻滞的自发恢复没有显著差异。然而，使用舒更葡糖时，较少患者出现AHVR残留抑制。在所有组中，相当一部分患者在恢复后40分钟仍存在AHVR的残留抑制。
原始文献：Snoek MAJ, van Lemmen MA, van der Schrier R, et al. Recovery of the Acute Hypoxic Ventilatory Response after Reversal of a Minimal Neuromuscular Block: A Randomized Controlled Trial in Healthy, Nonobese Volunteers. Anesthesiology. 2025 Oct 1;143(4):873-882. doi: 10.1097/ALN.0000000000005650. Epub 2025 Jul 11. PMID: 40644393; PMCID: PMC12416893.
Recovery of the Acute Hypoxic Ventilatory Response after Reversal of a Minimal Neuromuscular Block: A Randomized Controlled Trial in Healthy, Nonobese Volunteers
ABSTRACT
Background: Neuromuscular blocking agents inhibit the peripheral chemoreflex. This study examined the effect of 2 and 4 mg/kg sugammadex compared to spontaneous recovery of neuromuscular block on the recovery of the acute hypoxic ventilatory response (AHVR).
Methods: This was a two-experiment, randomized, controlled trial in healthy volunteers. Participants received a continuous infusion of rocuronium, to achieve stable symptoms of neuromuscular block in the head and neck region (symptomatic neuromuscular block). Thereafter, neuromuscular block was allowed to recover spontaneously in the first experiment, while in experiment 2, volunteers were randomized to receive 2 mg/kg or 4 mg/kg sugammadex for reversal. The depth of neuromuscular block was assessed with electromyography at the adductor pollicis muscle. AHVR was measured at baseline, during stable neuromuscular block, and at 0, 20, and 40 min after recovery.
Results: A total of 37 volunteers were enrolled; data from 27 volunteers were eligible for analysis. AHVR was reduced by 32% (mean difference vs. baseline, -0.22 l · % -1 · min -1 ; 95% CI, -0.32 to -0.12) during symptomatic neuromuscular block (mean train-of-four ratio, 0.42 ± 0.22;). At the disappearance of all symptoms, AHVR remained on average depressed by 23% (mean difference, -0.16 l · % -1 · min -1 ; 95% CI, -0.28 to -0.04). In 57% of volunteers after spontaneous recovery versus 28% after sugammadex reversal, AHVR did not return to baseline values during the measurement period. In addition, the magnitude of residual AHVR depression was greater after spontaneous recovery compared to reversal with sugammadex. However, on average AHVR was not significantly different from baseline at 20 and 40 min after recovery in any group.
Conclusions: The AHVR after reversal of a minimal neuromuscular block with sugammadex did not significantly differ with spontaneous recovery of neuromuscular block. However, fewer patients had residual depression of AHVR when sugammadex was used. In all groups, a considerable proportion of patients had residual depression of the AHVR 40 min after recovery.