The substances causing vasoconstriction / V.E. Henderson.

  • Henderson, V. E. (Velyein Ewart), 1877-1945.
Date:
[1940?]
Catalogue details

Licence: Public Domain Mark

Credit: The substances causing vasoconstriction / V.E. Henderson. Source: Wellcome Collection.

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    Printed in U. S. A. THE SUBSTANCES CAUSING VASOCONSTRICTION V. E. HENDERSON Department of Pharmacology, University. of Toronto EPINEPHRINE THE name epinephrine was applied by Abel to the active principle which he isolated in 1897 and which was subsequently found to be a benzoyl derivative (1). This name was adopted by the American Medical As- sociation in place of the protected name adrenaline. The first of this group of substances was revealed by the experi- ments of Oliver and Schaffer (2) in 1894 with extracts of the suprarenal lands. In 1901 Aldrich and Takamine isolated the active principle and named it-adrenaline. Friedmann in 1906 obtained its structural formula. It was synthetized by Stoltz and Dakin in 1905. The studies of these workers made evident that other chemically related bodies pro- duced more or less similar actions as did those of Barger and Dale (3). Oliver and Schaffer showed quite clearly that an extract of the suprarenal glands caused contraction of the arteries and led to an in- crease in the beat of the auricles and ventricles. They further showed that the effect of the active principle was peripheral upon the organs themselves and not due to an action on the central nervous system. In the thirty-five years that have passed since the publication of their main paper, it has been established that the amount of epinephrine present normally in the blood stream is extremely small; how small we do not know. The figures of Stewart and Rogoff would suggest about 0.002 mgm. in the blood of a man, and it has been shown that its pres- ence is not necessary to maintain the blood pressure. It may be that even this small amount has some importance in cardiac metabolism, allowing the heart to do the same amount of work with a lower con- sumption of oxygen, as suggested by Gremels (4), who found this to occur when from 0.0026—-0.008 gamma per kem. per min. of epinephrine was infused into acat. In his experiments, increasing the amount three times led to an increased consumption of oxygen, but even this amount is far smaller than that which may be released in the dog by stimulation of the sciatic nerve. Cannon (5) estimates that in fright, pain and ~ asphyxia, as much as 0.001 mgm. per kgm. body weight per minute may be released reflexly from the gland. This result is approximately what might be expected from the intravenous injection in man of 0.5 ee. epinephrine hydrochloride, when a rise in blood pressure would occur. Samson Wright (6) reports that if 1.5 cc. of the solution of epinephrine hydrochloride be injected subcutaneously in man, it will produce an in- creased cardiac rate with increased minute volume, but with no in- 323
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