Abstract
Agent BZ is the code name for 3-quinuclidinyl benzilate, an anticholinergic ester of glycolic acid. BZ is a PCW agent described as an anticholinergic hallucinogen.
BZ is a competitive inhibitor of the effects of ACh acting at the postsynaptic muscarinic receptors in the PNS and CNS. In the PNS, this inhibition is observed in the muscle, autonomic ganglia, and exocrine glands.
BZ's ability to readily cross the blood-brain barrier causes mental status changes and delirium. BZ is one of the most potent anticholinergic psychotomimetics known with only small doses necessary to produce incapacitation.
BZ at single doses of less than 1 mg produces delirium lasting several days. BZ is usually disseminated as an aerosol, and the primary route of absorption is through the respiratory system.
Absorption also can occur through the skin or by gastrointestinal tract absorption. The pharmacologic activity of BZ is similar to atropine or scopolamine but with a much longer duration of action.
Physicochemical properties and biological effects of BZ are described. The effect is characterized by vegetative symptoms progressing to hallucinations.
Distribution of BZ in the body is preferably in the peripheral, followed by the CNS. Its mechanism of effect is based on its interaction with cholinergic receptors in the CNS and PNS, and the resulting lack of a neuromediator-ACh.
The antidotal effect against BZ intoxication is based on an increase of ACh levels caused by reversible cholinesterase inhibitors. From this group of compounds, physostigmine was used as the first antidote against BZ.
However, physostigmine has a very thin margin between its therapeutic and toxic doses. Therefore, new inhibitors were developed, and acridine derivatives were found to be the most promising.
From these compounds, 7-MEOTA was the most effective. It is less toxic than physostigmine and tacrine and its central effect is pronounced.
It was introduced in the Czech army as an antidote against BZ poisoning.