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2. Before the advent of cocaine atropine was consideredto be a reliable, slowly acting local anesthetic, forexample in the treatment of painful inflammations ofthe cornea, fissure in ano, cardialgia secondary togastric ulcer, etc.3. Uhlike atropine, which has a slightly stimulatingaction on the eye (hyperemia, or even inflammationwhen used in eye drops), homatropine has been foundto be entirely without stimulating properties*4. Homatropine is formed from mandelic acid and tropineunder the same conditions as atropine is formed fromtropic acid and tropine,5. Mandelic acid is intermediate between tropic acid andbenzoic acid:C 6 H 5 »CH»(CH 2 OH)*COOH C^CHOH-COOH CgH^COOHtropic acid mandelic acid benzoic acidI found that atropine had a weak though distinctparalyzing action on peripheral sensory fibers, but that inthe case of homatropine the action was quite obvious.On the other hand I determined that ecgonine, obtainedfrom cocaine by Dr. Lossen, who very kindly gave me asupply, was entirely devoid of anesthetic action. It wasthus obvious that the anesthetizing principle in cocainecould not be ecgonine as such, but that activity depended onits combination with benzoic acid.We therefore propose provisionally - but entirelytentatively - that the conjunction with benzoic acid is theeffective factor. We take into account that the conjunction** In experimental tests one must allow for the greaterdiffusibility of homatropine. Compared with atropine,homatropine is removed much more quickly from the site ofapplication by the blood stream. Consequently, if onefails to eliminate the effect of the circulation, onemay often conclude erroneously that atropine is the moreactive drug. Experiments on frogs must therefore beperformed with prior removal of the heart, as well asthe brain.