Figure 3

Xenon is neuroprotective in a variety of mammalian in vitro and in vivo models. (a) Xenon treatment after cardiopulmonary resuscitation reduces neurological deficit in a pig model. There is a significant improvement in the neurological deficit score (NDS) in xenon-treated animals. †P < 0.01, *P < 0.05. (b) Xenon reduces infarct volume after focal ischemia in mice. Infarct volume after transient middle cerebral artery occlusion is significantly reduced in xenon-treated animals compared with those treated with nitrous oxide. NS, not significant. (c) Xenon improves neurological function following cardiopulmonary bypass (CPB) in a rat model. Xenon-treated animals received 60% xenon during CPB procedure. *P < 0.05, **P < 0.01, ***P < 0.001. (d) Xenon is neuroprotective in an in vitro model of traumatic brain injury. Xenon (75%) give significant neuroprotection (P < 0.05) when applied immediately after the trauma (grey bars) or after a delay of 2 or 3 hours (white bars). Xenon is particularly effective at reducing the secondary injury that develops in the 72 hours following injury. Figures adapted from: (a) Fries and colleagues [78], (b) Homi and colleagues [5], (c) Ma and colleagues [75], and (d) Coburn and colleagues [77].