British journal of clinical pharmacology · 2026
Effect of dexmedetomidine on cerebral homeostasis in patients undergoing craniotomy for brain tumour excision: A randomized double-blind trial.
СтатьяРандомизированное исследованиеНазвание и аннотация: Перевод в очереди
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Nikopoulou Anastasia, Grosomanidis Vasileios, Poulopoulou Aikaterina, Vyzantiadis Timoleon-Achilleas, Pourzitaki Chryssa, Patsalas Ioannis, Tsaousi Georgia G
Аннотация
AIM: Dexmedetomidine (DEX) seems to hold a potential neuroprotective role, possibly mediated by the attenuation of oxidative stress and neuroinflammation. This study aimed to delineate the effect of DEX used as an adjunct anaesthetic on cerebral oxygenation, cerebral injury and the release of inflammatory markers in brain tumour surgery.
METHODS: Fifty-six patients undergoing craniotomy for brain tumour excision were randomly assigned to receive either DEX (1 μg/kg for 10 min and thereafter 0.7 μg/kg/h) or placebo. Arterial and jugular-bulb blood samples were collected at predefined time-points, whereas a concomitant hemodynamic profile was obtained intraoperatively. S100B protein, neuron-specific enolase (NSE), tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6) and cortisol levels were determined at baseline and 6 and 24 h postoperatively.
RESULTS: Demographic and perioperative characteristics were comparable between groups. Propofol consumption was considerably reduced in DEX-treated patients (p < 0.001). Measured (jugular-bulb oxygen saturation and partial pressure of oxygen) and estimated (oxygen and carbon dioxide arterial-jugular differences, brain oxygen extraction ratio) cerebral oxygenation indices were favourably affected by DEX infusion (p < 0.05), yet this effect was valid for 15 min (p < 0.05), corresponding to transient systemic hemodynamic augmentation. Moreover, postoperative S100B, NSE, TNF-α, IL-6 and cortisol levels were significantly attenuated in the DEX group (p < 0.01).
CONCLUSION: DEX may attenuate the release of cerebral injury and neuroinflammation biomarkers and transiently improve hemodynamics and cerebral oxygenation during brain tumour surgery. Nonetheless, these surrogate effects do not establish clinically relevant neuroprotection, and potential dose-related hemodynamic instability warrants cautious, individualized use.
METHODS: Fifty-six patients undergoing craniotomy for brain tumour excision were randomly assigned to receive either DEX (1 μg/kg for 10 min and thereafter 0.7 μg/kg/h) or placebo. Arterial and jugular-bulb blood samples were collected at predefined time-points, whereas a concomitant hemodynamic profile was obtained intraoperatively. S100B protein, neuron-specific enolase (NSE), tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6) and cortisol levels were determined at baseline and 6 and 24 h postoperatively.
RESULTS: Demographic and perioperative characteristics were comparable between groups. Propofol consumption was considerably reduced in DEX-treated patients (p < 0.001). Measured (jugular-bulb oxygen saturation and partial pressure of oxygen) and estimated (oxygen and carbon dioxide arterial-jugular differences, brain oxygen extraction ratio) cerebral oxygenation indices were favourably affected by DEX infusion (p < 0.05), yet this effect was valid for 15 min (p < 0.05), corresponding to transient systemic hemodynamic augmentation. Moreover, postoperative S100B, NSE, TNF-α, IL-6 and cortisol levels were significantly attenuated in the DEX group (p < 0.01).
CONCLUSION: DEX may attenuate the release of cerebral injury and neuroinflammation biomarkers and transiently improve hemodynamics and cerebral oxygenation during brain tumour surgery. Nonetheless, these surrogate effects do not establish clinically relevant neuroprotection, and potential dose-related hemodynamic instability warrants cautious, individualized use.