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the quest for a therapeutic to ameliorate ischemic and traumatic brain injury is certainly a noble ideal , but , thus far , a futile endeavor . in the previous issue of critical care , loetscher and colleagues  
provided further evidence that the inert , noble gases may have ameliorative properties in the setting of acute neuronal injury .
stimulated by a shared interest in the neuroprotective properties of another noble gas , xenon [ 2 - 4 ] , they have shifted their focus to argon , a gas that is more abundant and cheaper to obtain . in their current investigation , they demonstrate that argon is neuroprotective when applied after an oxygen - glucose deprivation ( ogd ) or traumatic injury in organotypic hippocampal slice cultures in vitro . the models the authors employ are robust ; the cultured slices have intact synaptic networks , replicating the in vivo setting well ; ogd is a well - described simulation of ischemic brain injury ; similarly , the trauma model replicates the clinical situation .
loetscher and colleagues report a dose - responsive neuroprotective effect , with 50% argon appearing to be the optimal concentration for neuroprotection . furthermore , argon was even neuroprotective when administered 3 hours after the injury .
although this report used only in vitro models , it is a foundation on which to base further studies that may further reveal argon 's potential in a field largely bereft of interventions to improve neurological outcome from ischemic or traumatic brain injury .
we recently reported that argon ( 75% ) prevented neuronal injury from ogd in vitro but that the protection afforded was inferior to that of xenon .
xenon has been shown to be neuroprotective in multiple models and species and has now entered clinical trials for neonatal hypoxic - ischemic brain injury ( tobyxe ; nct00934700 ) . if argon is also to be exploited clinically , it too must undergo rigorous examination in different animal models , species , laboratories , and clinically relevant injury settings .
while at this stage argon fulfills some criteria , it would be imprudent , in the absence of in vivo data , to hail argon as the elusive neuroprotective agent .
why has there been a cascade of studies exploring the clinical utility of noble gases [ 1 - 5 	 , 7,8 ] ?
helium , neon , argon , krypton and xenon , the first five noble gases in the periodic table , contain a full outer shell of electrons , precluding the formation of covalent bonds under biological conditions ; thus , they are chemically inert . due to the uncharged and non - polar nature of their chemical composition , these gases are able to easily partition into the brain and are able to fit snugly into amphiphilic binding cavities within proteins . depending on the properties of the surrounding electrons , some of the noble gases can create an instantaneous dipole in the atom from a charged binding site , thereby promoting a biological effect , including induction of anesthesia .
neon and helium are thought to create an unfavorable balance between binding energies and repulsive forces and therefore do not produce anesthesia and other biological effects .
in the case of xenon , there are several candidate molecules that may be capable of producing the cytoprotective properties , including the nmda ( n - methyld- aspartic acid ) subtype of the glutamate receptor , the atp - sensitive potassium channel , the two - pore potassium channel , and an as - yet - unidentified protein that is upstream of mtor ( mammalian target of rapamycin ) . a reduced ability
to form induced dipoles with argon ( due to its smaller size ) may limit the number of available protein - binding sites when compared with xenon .
indeed , there are important pharmacodynamic differences between xenon and argon ; in particular , xenon is an anesthetic at atmospheric pressure , argon is not . nonetheless , argon 's lack of sedative properties may actually be beneficial as it allows administration to patients with acute , focal neurological injury ( such as stroke ) , who would not necessarily benefit from sedation .
xenon 's cost necessitates administration through cumbersome recirculating and recycling systems ; argon is substantially cheaper and thus may be feasibly administered through open circuits .
however , a decade of investigation of the effects of xenon has led to a clinical trial that may yet change clinical care of perinatal asphyxia .
the findings of loetscher and colleagues should encourage the pursuit of argon as a neuroprotective alternative / supplement to xenon .
mm has received consultancy fees and funding from air products ( allentown , pa , usa ) and air liquide sant international ( paris , france ) concerning the development of clinical applications for medical gases , including xenon .
rds has received consultancy fees from air liquide sant international concerning the development of clinical applications for xenon .
certain noble gases , though inert , exhibit remarkable biological properties . 
 notably , xenon and argon provide neuroprotection in animal models of central nervous system injury . in the previous issue of critical care , loetscher and 
 colleagues provided further evidence that argon may have therapeutic properties for neuronal toxicity by demonstrating protection against both traumatic and oxygen - glucose deprivation injury of organotypic hippocampal cultures in vitro . 
 their data are of interest as argon is more abundant , and therefore cheaper , than xenon ( the latter of which is currently in clinical trials for perinatal hypoxic - ischemic brain injury ; tobyxe ; nct00934700 ) . 
 we eagerly await in vivo data to complement the promising in vitro data hailing argon neuroprotection .