B deficiency. It inactivates the cobalamin form of vitamin B by oxidation. Symptoms of vitamin B deficiency, including sensory neuropathy, myelopathy and encephalopathy, may occur within days or weeks of exposure to nitrous oxide anaesthesia in people with subclinical vitamin B deficiency. Symptoms are treated with high doses of vitamin B, but recovery can be slow and incomplete. People with normal vitamin B levels have stores to make the effects of nitrous oxide insignificant, unless exposure is repeated and prolonged (nitrous oxide abuse). Vitamin B levels should be checked in people with risk factors for vitamin B deficiency prior to using nitrous oxide anaesthesia. Prenatal development Several experimental studies in rats indicate that chronic exposure of pregnant females to nitrous oxide may have adverse effects on the developing fetus. Chemical/physical risks At room temperature () the saturated vapour pressure is 50.525 bar, rising up to 72.45 bar at —the critical temperature. The pressure curve is thus unusually sensitive to temperature. As with many strong oxidisers, contamination of parts with fuels have been implicated in rocketry accidents, where small quantities of nitrous/fuel mixtures explode due to "water hammer"-like effects (sometimes called "dieseling"—heating due to adiabatic compression of gases can reach decomposition temperatures). Some common building materials such as stainless steel and aluminium can act as fuels with strong oxidisers such as nitrous oxide, as can contaminants that may ignite due to adiabatic compression. There also have been incidents where nitrous oxide decomposition in plumbing has led to the explosion of large tanks. Mechanism of action The pharmacological mechanism of action of in medicine is not fully known. However, it has been shown to directly modulate a broad range of ligand-gated ion channels, and this likely plays a major role in many of its effects. It moderately blocks NMDAR and β-subunit-containing nACh channels, weakly inhibits AMPA, kainate, GABA and 5-HT receptors, and slightly potentiates GABA and glycine receptors. It also has been shown to activate two-pore-domain channels. While affects quite a few ion channels, its anaesthetic, hallucinogenic and euphoriant effects are likely caused predominantly, or fully, via inhibition of NMDA receptor-mediated currents. In addition to its effects on ion channels, may act to imitate nitric oxide (NO) in the central nervous system, and this may be related to its analgesic and anxiolytic properties. Nitrous oxide is 30 to 40 times more soluble than nitrogen. The effects of inhaling sub-anaesthetic doses of nitrous