WHEN TAINTER, Tullar, and Luduena 1 reported, in 1948, the successful synthesis of levoarterenol, a smouldering controversy flared anew. Since Oliver and Shaefer,2 in 1895, observed that extracts of the adrenal medulla gave a vasopressor effect when administered intravenously to animals, a host of investigators have interested themselves in the apparent paradox of the inhibitory action of epinephrine in minimal amounts as compared with an excitatory action in larger amounts. Barger and Dale,3 in 1910, speculated that the sympathetic effector substance might not be epinephrine but, rather, a closely related catechol with a primary amine side-chain. Cannon4 proposed the concept of two forms of sympathetic effector substances, an inhibitor and an excitor form, which he called sympathin I and sympathin E, respectively. Bacq5 suggested the possibility that arterenol might be sympathin E, and Blaschko6 postulated that arterenol might be the precursor of epinephrine. In recent
SANDERSON GM, HUBBARD RS. QUALITATIVE DIFFERENCE BETWEEN LEVOEPINEPHRINE AND LEVOARTERENOL: Experimental Demonstration. AMA Arch Surg. 1953;67(5):746–752. doi:10.1001/archsurg.1953.01260040757013
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