Sleep medicine · 2025
Effects of dexmedetomidine and propofol on the key endotypes of OSA: A randomized, single-blind, placebo-controlled, crossover trial.
СтатьяРандомизированное исследованиеПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Li Chunbo, Fan Haiting, Duan Yujuan, Wang Dan, Lin Yang, Xin Wenjun, Ma Renqiang, Wen Weiping, Wu Yan
Аннотация
BACKGROUND: Drug-induced sleep has been shown to facilitate the diagnosis of obstructive sleep apnea (OSA). However, the effects of commonly used sedatives, such as dexmedetomidine and propofol, on the endotypic traits of OSA remained unclear.
OBJECTIVE: We aim to investigate the impact of dexmedetomidine and propofol on OSA endotypic traits.
METHODS: We conducted a randomized, single-blind, placebo-controlled, crossover trial in adult patients with OSA, comparing the OSA endotypic traits and polysomnography parameters among the interventions of placebo, dexmedetomidine and propofol.
RESULTS: 16 patients completed the trial and were enrolled for analysis. Both dexmedetomidine and propofol worsened pharyngeal collapsibility as indicated by a lower Vpassive (mean difference: 6.1 [95 % CI -9.1 to -3.0]%eupnea for dexmedetomidine versus placebo, p = 0.040; -16.5 [95 % CI -24.1 to -9.0]%eupnea for propofol versus placebo, p < 0.001), with propofol causing a greater effect (-10.4 [95 % CI -17.8 to -3.2]%eupnea for propofol versus dexmedetomidine, p < 0.001). Dexmedetomidine maintained upper airway gain, while propofol diminished it compared to placebo (p = 0.001). Both dexmedetomidine and propofol increased arousal threshold (p = 0.006 and p < 0.001, respectively). Dexmedetomidine had no effect on loop gain, whereas propofol elevated it (p = 0.004). Compared to placebo, dexmedetomidine had no impact on apnea-hypopnea index (AHI) or saturation of peripheral oxygen (SpO2). During propofol sedation, AHI in stages N1 (p < 0.001), N2 (p < 0.001) and the entire NREM (p = 0.038) sleep showed increases, and nadir SpO2 for NREM stage exhibited a decrease (p = 0.006).
CONCLUSIONS: Dexmedetomidine had less impact on OSA endotypic traits compared to propofol, and had no negative effects on AHI and SpO2.
OBJECTIVE: We aim to investigate the impact of dexmedetomidine and propofol on OSA endotypic traits.
METHODS: We conducted a randomized, single-blind, placebo-controlled, crossover trial in adult patients with OSA, comparing the OSA endotypic traits and polysomnography parameters among the interventions of placebo, dexmedetomidine and propofol.
RESULTS: 16 patients completed the trial and were enrolled for analysis. Both dexmedetomidine and propofol worsened pharyngeal collapsibility as indicated by a lower Vpassive (mean difference: 6.1 [95 % CI -9.1 to -3.0]%eupnea for dexmedetomidine versus placebo, p = 0.040; -16.5 [95 % CI -24.1 to -9.0]%eupnea for propofol versus placebo, p < 0.001), with propofol causing a greater effect (-10.4 [95 % CI -17.8 to -3.2]%eupnea for propofol versus dexmedetomidine, p < 0.001). Dexmedetomidine maintained upper airway gain, while propofol diminished it compared to placebo (p = 0.001). Both dexmedetomidine and propofol increased arousal threshold (p = 0.006 and p < 0.001, respectively). Dexmedetomidine had no effect on loop gain, whereas propofol elevated it (p = 0.004). Compared to placebo, dexmedetomidine had no impact on apnea-hypopnea index (AHI) or saturation of peripheral oxygen (SpO2). During propofol sedation, AHI in stages N1 (p < 0.001), N2 (p < 0.001) and the entire NREM (p = 0.038) sleep showed increases, and nadir SpO2 for NREM stage exhibited a decrease (p = 0.006).
CONCLUSIONS: Dexmedetomidine had less impact on OSA endotypic traits compared to propofol, and had no negative effects on AHI and SpO2.