Pharmacotherapeutic group: Psycholeptics: Other hypnotics and sedatives: Bromides.
ATCvet code: QN05CM11
Pharmacodynamic properties
Potassium bromide is a halide anticonvulsant. Bromide replaces chloride in all body fluids. It competes with chloride transport across nerve cell membranes and inhibits sodium transport and so causes membrane hyperpolarisation. This hyperpolarisation raises the seizure threshold and prevents the spread of epileptic discharges. Bromide has effects on active transport across glial cell membranes and affects passive movements of ions by competition with chloride for anion channels in post-synaptic membranes that are activated by inhibitory neurotransmitters. This potentiates the effect of GABA which results in a synergistic activity of bromide with other drugs that have GABA-ergic activity.
Pharmacokinetic particulars
The pharmacokinetics of potassium bromide have been studied in dogs. The half-life is approximately 24 days. Due to this extremely long half-life, it can take several weeks/months to achieve steady state concentrations. Potassium bromide is well absorbed orally with peak absorption in about 1.5 hours. Once ingested, the potassium bromide salt dissociates, and the bromide ion is rapidly absorbed by the gastrointestinal tract.
After absorption, the bromide ion rapidly distributes, as does chloride, throughout the extra-cellular space and into cells. Chloride is distributed passively across most cell membranes according to the trans-membrane potential, and it is likely that bromide distributes in the same manner. As the bromide concentration is increased in the body, the concentration of chloride is decreased in direct proportion to the increase in bromide.
Bromide is not metabolised by the body, it enters and leaves the body only as the monovalent anion. Excretion of bromide is mainly via the kidneys, where it competes with chloride for tubular reabsorption.