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![Figure 2.](/view/journals/anpr/62/2/inline-i0003-3006-62-2-57-f02.png)
Response to use of nonsteroidal analgesics. *Ibuprofen and celecoxib, respectively, were considered analgesics separately. †There was no information available about the choice of patient by better response to NSAID or placebo used. Data represent the number of patients who did not make use of supplementary rescue analgesia.
![Figure 1.](/view/journals/anpr/54/1/inline-i0003-3006-54-1-9-f01.gif)
Mechanism of N2O-induced analgesia. N2O is thought to stimulate the neuronal release of endogenous opioid peptide or dynorphins (DYNs); the molecular aspects of how N2O initiates this process are as yet unknown. The pre-synaptic nerve terminal takes up L-arginine (L-Arg), which is converted by the enzyme nitric oxide synthase (NOS) to L-citrulline (L-Cit) and nitric oxide (NO). NO appears to be involved in the stimulated release of DYNs. DYNs traverse the synaptic cleft and activate postsynaptic opioid receptors, which belong to the 7-transmembrane–spanning, G protein–coupled superfamily of receptors.
![Figure 1.](/view/journals/anpr/58/1/inline-i0003-3006-58-1-14-f01.png)
Number of “anesthesia and analgesia” articles by decade.
![Figure 2.](/view/journals/anpr/58/1/inline-i0003-3006-58-1-14-f02.png)
Number of “anesthesia and analgesia” and “dentistry” articles by decade.