Related theory

Nitrous oxide has been used in clinical practice for over 150 years. The exact mechanism of action of nitrous oxide has never been fully understood (Emmanouil and Quock [64]). Research suggests that its mode of action is due to a release of endogenous opioid peptide that then activates opioid receptors and the descending GABA and noradrenergic pathways; this then modulates pain response in the spinal cord (Emmanouil and Quock [64]).
N‐methyl‐D‐aspartate (NMDA) receptor currents are inhibited by nitrous oxide and it is known that these receptors are involved with many CNS pathways (Jevtovic‐Todorovic et al. [112]). The release of these neurotransmitters is thought to activate descending pain pathways which modulate pain transmission in the spinal cord (Maze and Fujinaga [137]). Pulmonary transfer of nitrous oxide is rapid, with onset of effect in seconds and full analgesic effect within 1–2 minutes. It is also rapidly eliminated from the blood, via the lungs, when inhalation ceases (Trojan et al. [217]).