adding helium to the lasing medium. The first excimer laser used a xenon dimer (Xe2) energized by a beam of electrons to produce stimulated emission at an ultraviolet wavelength of 176 nm. Xenon chloride and xenon fluoride have also been used in excimer (or, more accurately, exciplex) lasers. Medical Anesthesia Xenon has been used as a general anesthetic, but it is more expensive than conventional anesthetics. Xenon interacts with many different receptors and ion channels, and like many theoretically multi-modal inhalation anesthetics, these interactions are likely complementary. Xenon is a high-affinity glycine-site NMDA receptor antagonist. However, xenon is different from certain other NMDA receptor antagonists in that it is not neurotoxic and it inhibits the neurotoxicity of ketamine and nitrous oxide (N2O), while actually producing neuroprotective effects. Unlike ketamine and nitrous oxide, xenon does not stimulate a dopamine efflux in the nucleus accumbens. Like nitrous oxide and cyclopropane, xenon activates the two-pore domain potassium channel TREK-1. A related channel TASK-3 also implicated in the actions of inhalation anesthetics is insensitive to xenon. Xenon inhibits nicotinic acetylcholine α4β2 receptors which contribute to spinally mediated analgesia. Xenon is an effective inhibitor of plasma membrane Ca2+ ATPase. Xenon inhibits Ca2+ ATPase by binding to a hydrophobic pore within the enzyme and preventing the enzyme from assuming active conformations. Xenon is a competitive inhibitor of the serotonin 5-HT3 receptor. While neither anesthetic nor antinociceptive, this reduces anesthesia-emergent nausea and vomiting. Xenon has a minimum alveolar concentration (MAC) of 72% at age 40, making it 44% more potent than N2O as an anesthetic. Thus, it can be used with oxygen in concentrations that have a lower risk of hypoxia. Unlike nitrous oxide, xenon is not a greenhouse gas and is viewed as environmentally friendly. Though recycled in modern systems, xenon vented to the atmosphere is only returning to its original source, without environmental impact. Neuroprotectant Xenon induces robust cardioprotection and neuroprotection through a variety of mechanisms. Through its influence on Ca2+, K+, KATP\HIF, and NMDA antagonism, xenon is neuroprotective when administered before, during and after ischemic insults. Xenon is a high affinity antagonist at the NMDA receptor glycine site. Xenon is cardioprotective in ischemia-reperfusion conditions by inducing pharmacologic non-ischemic preconditioning. Xenon is cardioprotective by activating PKC-epsilon and downstream p38-MAPK. Xenon mimics neuronal ischemic preconditioning by activating ATP sensitive potassium channels. Xenon allosterically reduces ATP mediated channel activation inhibition independently of the sulfonylurea receptor1 subunit, increasing