Background <p>Although the anesthetized brain retains basic auditory function, the impact of intraoperative sound on recovery remains unclear. This study employed a translational approach to assess how different auditory environments influence recovery and associated neuroplasticity markers following general anesthesia.</p> Methods <p>A clinical trial randomized 129 surgical patients to control, music, or noise-canceling conditions, recording anesthesia time, PACU stay, and delirium. In parallel, a rat model of propofol anesthesia with incision pain was exposed to control, noise, or denoise settings. Induction and emergence were measured via righting reflex, while behavior was assessed postoperatively using open-field and Y-maze tests. Neuroplasticity markers (KCC2, c-Fos, GABRA1, BDNF) were quantified in key brain regions (hippocampus, prefrontal cortex, and thalamus) exclusively in the rat model and measured in brain tissue samples.</p> Results <p>Clinically, noise cancellation shortened PACU stay and reduced delirium incidence on the third day. In animals, noise exposure paradoxically hastened anesthesia recovery but led to a pathological “stress-arousal” phenotype marked by hypoactivity and anxiety-like behavior. This phenomenon was associated with disrupted thalamocortical inhibition, evidenced by downregulated mRNA expression of KCC2 and c‑Fos alongside elevated levels of GABRA1 and BDNF—a molecular profile suggestive of excitotoxic, rather than restorative, arousal.</p> Conclusion <p>The intraoperative auditory environment strongly modulates recovery quality. Excessive noise drives a maladaptive stress-arousal state linked to inhibitory homeostasis disruption, indicating that operating room quiet should be considered a neuroprotective intervention rather than merely an environmental courtesy.</p> <p><i>Trial registration</i> PID:242329 (ID: ChiCTR2400091050). Registered in ClinicalTrials.gov on 19 October 2024—Retrospectively registered, <a href="https://www.chictr.org.cn/bin/project/edit?pid=242329">https://www.chictr.org.cn/bin/project/edit?pid=242329</a></p>

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Intraoperative auditory environment affects general anesthesia recovery quality: insights from clinical and translational evidence

  • Haibin Zhang,
  • Boya Wang,
  • Yang Yang,
  • Jieping Lv,
  • Yizhuo Liu,
  • Jing Jia,
  • Ping Wu,
  • Qingping Wen

摘要

Background

Although the anesthetized brain retains basic auditory function, the impact of intraoperative sound on recovery remains unclear. This study employed a translational approach to assess how different auditory environments influence recovery and associated neuroplasticity markers following general anesthesia.

Methods

A clinical trial randomized 129 surgical patients to control, music, or noise-canceling conditions, recording anesthesia time, PACU stay, and delirium. In parallel, a rat model of propofol anesthesia with incision pain was exposed to control, noise, or denoise settings. Induction and emergence were measured via righting reflex, while behavior was assessed postoperatively using open-field and Y-maze tests. Neuroplasticity markers (KCC2, c-Fos, GABRA1, BDNF) were quantified in key brain regions (hippocampus, prefrontal cortex, and thalamus) exclusively in the rat model and measured in brain tissue samples.

Results

Clinically, noise cancellation shortened PACU stay and reduced delirium incidence on the third day. In animals, noise exposure paradoxically hastened anesthesia recovery but led to a pathological “stress-arousal” phenotype marked by hypoactivity and anxiety-like behavior. This phenomenon was associated with disrupted thalamocortical inhibition, evidenced by downregulated mRNA expression of KCC2 and c‑Fos alongside elevated levels of GABRA1 and BDNF—a molecular profile suggestive of excitotoxic, rather than restorative, arousal.

Conclusion

The intraoperative auditory environment strongly modulates recovery quality. Excessive noise drives a maladaptive stress-arousal state linked to inhibitory homeostasis disruption, indicating that operating room quiet should be considered a neuroprotective intervention rather than merely an environmental courtesy.

Trial registration PID:242329 (ID: ChiCTR2400091050). Registered in ClinicalTrials.gov on 19 October 2024—Retrospectively registered, https://www.chictr.org.cn/bin/project/edit?pid=242329