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Alternative technique or mitigating strategy for sevoflurane-induced neurodegeneration: a randomized controlled dose-escalation study of dexmedetomidine in neonatal rats

Authors
 J.-R. Lee  ;  E.P. Lin  ;  R.D. Hofacer  ;  B. Upton  ;  S.Y. Lee  ;  L. Ewing  ;  B. Joseph  ;  A.W. Loepke 
Citation
 British Journal of Anaesthesia, Vol.119(3) : 492-505, 2017 
Journal Title
 British Journal of Anaesthesia 
ISSN
 0007-0912 
Issue Date
2017
Keywords
anaesthetics ; apoptosis ; brain injury ; dexmedetomidine ; inhalation ; neuroprotection ; safety ; sevoflurane ; toxicity
Abstract
Background: Brain injury in newborn animals from prolonged anaesthetic exposure has raised concerns for millions of children undergoing anaesthesia every yr. Alternative anaesthetic techniques or mitigating strategies are urgently needed to ameliorate potentially harmful effects. We tested dexmedetomidine, both as a single agent alternative technique and as a mitigating adjuvant for sevoflurane anaesthesia. Methods: Neonatal rats were randomized to three injections of dexmedetomidine (5, 25, 50, or 100 µg kg -1 every 2 h), or 6 h of 2.5% sevoflurane as a single agent without or with dexmedetomidine (1, 5, 10, or 20 µg kg -1 every 2 h). Heart rate, oxygen saturation, level of consciousness, and response to pain were assessed. Cell death was quantified in several brain regions. Results: Dexmedetomidine provided lower levels of sedation and pain control than sevoflurane. Exposure to either sevoflurane or dexmedetomidine alone did not cause mortality, but the combination of 2.5% sevoflurane and dexmedetomidine in doses exceeding 1 µg kg -1 did. Sevoflurane increased apoptosis in all brain regions; supplementation with dexmedetomidine exacerbated neuronal injury, potentially as a result of ventilatory or haemodynamic compromise. Dexmedetomidine by itself increased apoptosis only in CA2/3 and the ventral posterior nucleus, but not in prefrontal cortex, retrosplenial cortex, somatosensory cortex, subiculum, lateral dorsal thalamic nucleaus, or hippocampal CA1. Conclusions: We confirm previous findings of sevoflurane-induced neuronal injury. Dexmedetomidine, even in the highest dose, did not cause similar injury, but provided lesser degrees of anaesthesia and pain control. No mitigation of sevoflurane-induced injury was observed with dexmedetomidine supplementation, suggesting that future studies should focus on anaesthetic-sparing effects of dexmedetomidine, rather than injury-preventing effects.
URI
http://ir.ymlib.yonsei.ac.kr/handle/22282913/160934
DOI
10.1093/bja/aex219
Appears in Collections:
1. Journal Papers (연구논문) > 1. College of Medicine (의과대학) > Dept. of Anesthesiology and Pain Medicine (마취통증의학교실)
Yonsei Authors
이정림(Lee, Jeong Rim)
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Full Text
https://www.sciencedirect.com/science/article/pii/S0007091217537666
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