J. Sleigh

Ketamine is notorious for causing diverse central nervous system effects, and for its promiscuous binding to many different neuronal receptors. Indeed, ketamine is an established pharmacological model for schizophrenic psychosis.¹ In this issue of the British Journal of Anaesthesia, Jonkman² shows that it was possible to attenuate the psychedelic or psychotomimetic effects of racemic ketamine—but not those of its S(+)-enantiomer—by infusing a low dose of sodium nitroprusside. The underlying rationale is that the ketamine blockade of N-methyl-d-aspartate (NMDA) type glutamate receptors induces multiple downstream intracellular effects, primarily via blockade of Ca²⁺ entry.