In this section
Anaesthesia makes up the largest hospital speciality and has a huge role to play in nearly every aspect of any hospital from operating theatres to accident and emergency, to the labour ward, and to intensive care. Our research ranges from basic molecular research into mechanisms of anaesthesia to investigating the clinical impact of novel anaesthetic agents.
Our research covers the entirety of patient’s perioperative journey and through this, we aim to deliver the greatest impact. The section has been pioneering in the development of novel technologies to facilitate the delivery of anaesthetic agents and has also made pivotal in-roads into the mechanism of action of anaesthetic agents and their wider application to other diseases (such as their protective roles in brain injury and in cancer).
@article{Harris:2013:10.1097/ALN.0b013e3182a2a265.,
author = {Harris, K and Armstrong, SP and Campos-Pires, R and Kiru, L and Franks, NP and Dickinson, R},
doi = {10.1097/ALN.0b013e3182a2a265.},
journal = {Anesthesiology},
pages = {1137--1148},
title = {Neuroprotection against traumatic brain injury by xenon but not argon, is mediated by inhibition at the NMDA receptor glycine site},
url = {http://dx.doi.org/10.1097/ALN.0b013e3182a2a265.},
volume = {119},
year = {2013}
}
TY - JOUR
AB - Background. The inert anesthetic gas xenon is neuroprotective in models of brain injury. Weinvestigate the neuroprotective mechanisms of the inert gases xenon, argon, krypton, neon andhelium in an in vitro model of traumatic brain injury.Methods. We use an in vitro model using mouse organotypic hippocampal brain-slices, subjectedto a focal mechanical trauma, with injury quantified by propidium-iodide fluorescence. Patch-clampelectrophysiology is used to investigate the effect of the inert gases on N-methyl-D-aspartate(NMDA)-receptors and TREK-1 channels, two molecular targets likely to play a role inneuroprotection.Results. Xenon(50%) and, to a lesser extent, argon(50%) are neuroprotective against traumaticinjury when applied following injury [xenon 43±1% protection 72hours after injury (N=104); argon30±6% protection (N=44); mean±SEM]. Helium, neon and krypton are devoid of neuroprotectiveeffect. Xenon(50%) prevents development of secondary injury up to 48 hours after trauma.Argon(50%) attenuates secondary injury, but is less effective than xenon [xenon 50±5% reductionin secondary injury 72hours after injury (N=104); argon 34±8% reduction (N=44); mean±SEM].Glycine reverses the neuroprotective effect of xenon, but not argon, consistent with competitiveinhibition at the NMDA receptor glycine-site mediating xenon neuroprotection against traumaticbrain injury. Xenon inhibits NMDA receptors and activates TREK-1 channels, while argon,krypton, neon and helium have no effect on these ion-channels.Conclusions. Xenon neuroprotection against traumatic brain injury can be reversed by elevatingthe glycine concentration, consistent with inhibition at the NMDA-receptor glycine site playing asignificant role in xenon neuroprotection. Argon and xenon do not act via the same mechanism.
AU - Harris,K
AU - Armstrong,SP
AU - Campos-Pires,R
AU - Kiru,L
AU - Franks,NP
AU - Dickinson,R
DO - 10.1097/ALN.0b013e3182a2a265.
EP - 1148
PY - 2013///
SN - 1528-1175
SP - 1137
TI - Neuroprotection against traumatic brain injury by xenon but not argon, is mediated by inhibition at the NMDA receptor glycine site
T2 - Anesthesiology
UR - http://dx.doi.org/10.1097/ALN.0b013e3182a2a265.
UR - http://hdl.handle.net/10044/1/26435
VL - 119
ER -