Thomson Luke D J, Landry Shane A, Arellano Andre, Collet Jinny, Huddle Stuart, O'Driscoll Denise M, Mann Dwayne L, Beatty Caroline, Joosten Simon A, Hamilton Garun S, Berger Phillip J, Cooke Ian, Edwards Bradley A
Department of Physiology, School of Biomedical Sciences and Biomedical Discovery Institute, Monash University, Melbourne, VIC, Australia.
School of Psychological Science, Monash University, Melbourne, VIC, Australia.
J Physiol. 2025 May;603(10):3245-3260. doi: 10.1113/JP288337. Epub 2025 Apr 3.
Ventilatory control instability, or high loop gain (LG), contributes towards upper airway collapse in approximately one-third of people with obstructive sleep apnoea (OSA). A high LG can be the product of elevated chemosensitivity (controller gain) and/or an excessive ventilatory output (plant gain). Therapies such as carbonic anhydrase inhibitors (targeting plant gain) have been shown to reduce OSA severity; however, there is a lack of viable pharmacological options targeting controller gain. This study investigated the effect of flupirtine (400 mg), a KCNQ potassium channel opener, on LG and OSA severity in fifteen moderate-to-severe OSA patients through a randomised, double-blind, placebo-controlled trial. Despite the hypothesised potential of flupirtine to reduce LG by attenuating chemosensory activity, our findings revealed no significant effect on LG and OSA severity. The lack of overall efficacy of flupirtine is most likely due to multifactorial nature of OSA and the challenges of its management. Our findings suggest a need for a nuanced understanding of OSA pathogenesis and caution against the use of flupirtine in managing OSA. While, pharmacological modulation of ionic channels within the ventilatory control system presents a promising strategy, given the plethora of robust targets available, it remains to be determined whether an effective treatment can capitalise on a single predominant ionic current ubiquitous throughout the ventilatory system, or if a more successful approach necessitates the simultaneous modulation of multiple targets. This research enhances our understanding of the ventilatory control system's contribution to OSA and the complexity of finding a one-size-fits-all treatment. KEY POINTS: Around one-third of obstructive sleep apnoea (OSA) cases involve an unstable control of breathing, leading to airway collapse. This research examined whether the drug flupirtine could stabilise breathing control and reduce OSA severity in 15 patients. Flupirtine, which was expected to improve breathing control by reducing chemosensitivity, showed no significant benefit for OSA. While targeting ionic channels in the breathing system is promising, the search for an effective OSA treatment may require addressing multiple targets simultaneously.
通气控制不稳定,即高环路增益(LG),在大约三分之一的阻塞性睡眠呼吸暂停(OSA)患者中会导致上气道塌陷。高LG可能是化学敏感性升高(控制器增益)和/或通气输出过多(对象增益)的结果。诸如碳酸酐酶抑制剂(针对对象增益)等疗法已被证明可降低OSA的严重程度;然而,缺乏针对控制器增益的可行药理学选择。本研究通过一项随机、双盲、安慰剂对照试验,调查了钾通道开放剂氟吡汀(400毫克)对15例中重度OSA患者的LG和OSA严重程度的影响。尽管推测氟吡汀可能通过减弱化学感应活动来降低LG,但我们的研究结果显示其对LG和OSA严重程度无显著影响。氟吡汀总体缺乏疗效很可能是由于OSA的多因素性质及其管理方面的挑战。我们的研究结果表明,需要对OSA发病机制有细致入微的理解,并谨慎使用氟吡汀治疗OSA。虽然,对通气控制系统内离子通道的药理学调节是一种有前景的策略,但鉴于有大量可靠的靶点,能否通过利用整个通气系统中普遍存在的单一主要离子电流来实现有效治疗,或者更成功的方法是否需要同时调节多个靶点,仍有待确定。这项研究增进了我们对通气控制系统在OSA中的作用以及寻找一刀切治疗方法的复杂性的理解。要点:大约三分之一的阻塞性睡眠呼吸暂停(OSA)病例涉及呼吸控制不稳定,导致气道塌陷。本研究调查了药物氟吡汀是否能稳定15例患者的呼吸控制并降低OSA严重程度。预期通过降低化学敏感性来改善呼吸控制的氟吡汀,对OSA并无显著益处。虽然针对呼吸系统中的离子通道有前景,但寻找有效的OSA治疗方法可能需要同时针对多个靶点。