Tetraethylammonium (TEA) is a quaternary ammonium cation with the chemical formula [Et4N]+, consisting of four ethyl groups (−C2H5, denoted Et) attached to a central nitrogen atom.

[13] It is clear that TEA[14] blocks autonomic ganglia - it was the first "ganglionic blocker" drug to be introduced into clinical practice.

[25] Although TEA (sometimes under the name "Etamon"[26]) was explored in a number of different clinical applications,[16] including the treatment of hypertension,[27] its major use seems to have been as a probe to assess the capacity for vasodilation in cases of peripheral vascular disease.

[30] An extensive study of the toxicology of tetraethylammonium chloride in mice, rats and dogs was published by Gruhzit and co-workers in 1948.

[31] These investigators recorded the following acute toxicities, as LD50s for TEA chloride (error ranges not shown): Another research group, working at about the same time, but using tetraethylammonium bromide, published the following LD50 data:[32] Writing in 1950, Graham made some observations on the toxic effects of tetraethylammonium bromide in humans.

In one subject, described as a "healthy woman", 300 mg of tetraethylammonium bromide, i.v., produced incapacitating "curariform" (i.e., resembling the effects of tubocurarine) paralysis of the skeletal muscles, as well as marked drowsiness.

[28] Citing the work of other investigators, Graham noted that Birchall[30] had also produced "alarming curariform effects" in humans with i.v.