Sarin Gas

Like other organophosphate nerve agents, sarin inhibits the break down of the enzyme acetyl-cholinesterase. Under normal conditions, this enzyme hydrolyzes the neurotransmitter acetylcholine. When sarin is present, the build up of acetyl-cholinesterase results in the accumulation of excessive concentrations of acetylcholine in nerve synapses. This overstimulates parasympathetic nerves in the smooth muscle of the eyes, respiratory tract, gastrointestinal tract, sweat glands, cardiac muscles and blood vessels.

After exposure to sarin, symptoms begin within minutes. If a person survives for a few hours after exposure, he or she will likely recover from the poisoning. The first symptoms of sarin poisoning include a runny nose, blurred vision, sweating and muscle twitches. Longer exposures result in tightness of the chest, headache, cramps, nausea, vomiting, involuntary defecation and urination, convulsions, coma and respiratory arrest.

Atropine acts an antidote for nerve agent, including sarin. Atropine binds to one type of acetylcholine receptor on the post-synaptic nerve. A second antidote is pralidoxime iodide (PAM), which blocks sarin from binding to any free acetyl-cholinesterase. Both should be administered as soon as possible following exposure to the toxin. Diazapam can also be used to prevent seizures and convulsions. Soldiers fighting in regions where chemical weapons are likely to be deployed are now equipped with a Mark I antidote kit containing both atropine and PAM.