It is involved in the regulation of GABA, dopamine, 5-hydroxytryptamine, and acetylcholine. In monitored sedation, GHB decreases cardiac output due to slight decreases in stroke volume and heart rate. In the brain, GHB increases acetylcholine and affects the rate of serotonin metabolism. The precise function and metabolic pathways of GHB are complex and not yet fully understood. GHB is rapidly absorbed by oral, intravenous, and intraperitoneal routes.
Distribution is rapid, and the volume of distribution is small.
The primary effect of GHB is central nervous system depression. Its initial clinical use was therefore to induce anesthesia. It is still used in Europe as an adjunct for anesthesia. GHB induces a trancelike state that mimics physiologic sleep. Animal research demonstrated a potential for high doses to cause seizures.