GHB has a decades long track record of use as a general anesthetic. Administered intravenously, an anesthetic dose of GHB is in the range of 4-5 grams for a 150-pound person [Vickers, 1969]. Its advantages as an anesthetic include low toxicity, relatively few contraindications, slowing of the heart rate without loss of blood pressure, the absence of irritation to the veins with intravenous administration, muscle relaxation, absence of respiratory depression (usually), reduction of body temperature (hypothermia), and various protective and anti-shock actions [Laborit, 1964].
However, GHB can almost never be used in anesthesia without the additional administration of other drugs [Vickers, 1969] because it does not produce complete surgical anesthesia except in children [Laborit, 1964]. The autonomic nervous system remains active during GHB-induced anesthetic coma, and thus the body continues to respond to surgical stimuli through increases in heart rate, blood pressure, and cardiac output, as well as through sweating, peripheral vasoconstriction, vocalization, and reflex muscle action [Vickers, 1969]. Local anesthetics or other drugs which suppress these responses must therefore also be used, like the way a dentist or orthodontic surgeon might use Novocaine to kill pain along with nitrous oxide to render a patient unconscious. It is suspected that part of GHB’s protective function involves a slowing of the metabolism of brain cells, thus reducing their requirements for oxygen and glucose [Chin and Kreutzer, 1992; Artru, 1980]. Another factor in GHB’s anti-shock capability may be the marked vasodilation induced in the liver and kidney, thus increasing blood flow to those vital organs.
GHB’s efficacy for treating anxiety has been positively demonstrated in tests involving schizophrenic subjects [Laborit, 1964]. Its sedative properties have earned it a role as a psychotherapeutic adjunct [Vickers, 1969]. It has also been used to assist the process of “abreaction,” or the release (usually through verbalization) of repressed emotion [Vickers, 1969]. Unlike other “anxiolytic” (or anti-anxiety) drugs, GHB’s effect is non-toxic. Furthermore, GHB’s reduction of inhibitions, its tendency to encourage verbalization, and the typical lack of fear during the GHB experience would seem to provide an ideal context for the verbal exploration of difficult emotional territory during therapy.