Animal studies have demonstrated a strong neuroprotective property of xenon. Its usefulness in patients with cerebral pathology could be compromised by deleterious effects on regional cerebral blood flow (rCBF).
15O-labeled water was used to determine rCBF in nine healthy male subjects at baseline and during 1 minimum alveolar concentration (MAC) of xenon (63%). Anesthesia was based solely on xenon. Absolute changes in rCBF were quantified using region-of-interest analysis and voxel-based analysis.
Mean arterial blood pressure and arterial partial pressure for carbon dioxide remained unchanged. The mean (+/-SD) xenon concentration during anesthesia was 65.2+/-2.3%. Xenon anesthesia decreased absolute rCBF by 34.7+/-9.8% in the cerebellum (P<0.001), by 22.8+/-10.4% in the thalamus (P=0.001), and by 16.2+/-6.2% in the parietal cortex (P<0.001). On average, xenon anesthesia decreased absolute rCBF by 11.2+/-8.6% in the gray matter (P=0.008). A 22.1+/-13.6% increase in rCBF was detected in the white matter (P=0.001). Whole-brain voxel-based analysis revealed widespread cortical reductions and increases in rCBF in the precentral and postcentral gyri.
One MAC of xenon decreased rCBF in several areas studied. The greatest decreases were detected in the cerebellum, the thalamus and the cortical areas. Increases in rCBF were observed in the white matter and in the pre- and postcentral gyri. These results are in clear contradiction with ketamine, another N-methyl-D-aspartate antagonist and neuroprotectant, which induces a general increase in cerebral blood flow at anesthetic concentrations.
"We observed a departure from slow and temporally correlated dynamics in frontal regions and in the thalamus. These areas strongly overlap with those where decreased metabolism under anesthesia was reported (Alkire et al., 1997; Kaisti et al., 2002; Kaisti et al., 2003; Schreckenberger et al., 2004; Laitio et al., 2007; Bonhomme et al., 2008). Breakdown of longrange temporal correlations was also reported in other unconscious brain states such as deep non-rapid eye movement (NREM) sleep (Tagliazucchi et al., 2013a). "
[Show abstract][Hide abstract] ABSTRACT: Loss of cortical integration and changes in the dynamics of
electrophysiological brain signals characterize the transition from wakefulness
towards unconsciousness. The common mechanism underlying these observations
remains unknown. In this study we arrive at a basic model, which explains these
empirical observations based on the theory of phase transitions in complex
systems. We studied the link between spatial and temporal correlations of
large-scale brain activity recorded with functional magnetic resonance imaging
during wakefulness, propofol-induced sedation and loss of consciousness, as
well as during the subsequent recovery. We observed that during unconsciousness
activity in frontal and thalamic regions exhibited a reduction of long-range
temporal correlations and a departure of functional connectivity from the
underlying anatomical constraints. These changes in dynamics and
anatomy-function coupling were correlated across participants, suggesting that
temporal complexity and an efficient exploration of anatomical connectivity are
inter-related phenomena. A model of a system exhibiting a phase transition
reproduced our findings, as well as the diminished sensitivity of the cortex to
external perturbations during unconsciousness. This theoretical framework
unifies different empirical observations about brain activity during
unconsciousness and predicts that the principles we identified are universal
and independent of the causes behind loss of awareness.
"A recent study by Laitio et. al.  showed that administration of xenon (63%) in humans decreased rCBF in the cerebellum, thalamus, and cortical areas, while increasing rCBF in white matter and in parts of the precentral and postcentral gyri. Based on work by Rex et. "
[Show abstract][Hide abstract] ABSTRACT: In hyperpolarized xenon magnetic resonance imaging (HP (129)Xe MRI), the inhaled spin-1/2 isotope of xenon gas is used to generate the MR signal. Because hyperpolarized xenon is an MR signal source with properties very different from those generated from water-protons, HP (129)Xe MRI may yield structural and functional information not detectable by conventional proton-based MRI methods. Here we demonstrate the differential distribution of HP (129)Xe in the cerebral cortex of the rat following a pain stimulus evoked in the animal's forepaw. Areas of higher HP (129)Xe signal corresponded to those areas previously demonstrated by conventional functional MRI (fMRI) methods as being activated by a forepaw pain stimulus. The percent increase in HP (129)Xe signal over baseline was 13-28%, and was detectable with a single set of pre and post stimulus images. Recent innovations in the production of highly polarized (129)Xe should make feasible the emergence of HP (129)Xe MRI as a viable adjunct method to conventional MRI for the study of brain function and disease.
PLoS ONE 07/2011; 6(7):e21607. DOI:10.1371/journal.pone.0021607 · 3.23 Impact Factor
"In rat brain synaptic plasma membranes, xenon inhibits plasma membrane calcium ATPase pump activity, resulting in an increase in neuronal Ca2+ concentration and an altered excitability in these cells . The decrease in regional CBF after xenon treatment  may help reduce intracranial pressure, and the regional cerebral metabolic rate for glucose . "
[Show abstract][Hide abstract] ABSTRACT: Medical gases are pharmaceutical molecules which offer solutions to a wide array of medical needs. This can range from use in burn and stroke victims to hypoxia therapy in children. More specifically however, gases such as oxygen, helium, xenon, and hydrogen have recently come under increased exploration for their potential theraputic use with various brain disease states including hypoxia-ischemia, cerebral hemorrhages, and traumatic brain injuries. As a result, this article will review the various advances in medical gas research and discuss the potential therapeutic applications and mechanisms with regards to the field of neurobiology.
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