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Abstract
In this comparative study of cobefrin and epinephrine, it has been shown that these
two substances have many properties in common, and that, for the most part, their
physiologic behavior is identical. There are, however, several differences which are
noteworthy. Both substances produce similar increases in the blood pressure of test
animals, with the exception that the activity of cobefrin generally endures slightly
longer than that of epinephrine. The duration of the pressor response produced by
comparable doses of cobefrin is midway between that of epinephrine and ephedrine.
Epinephrine causes a more marked but shorter pressor response than does ephedrine.
Cobefrin gives the same abrupt pressor response as does epinephrine; the pressor response
of cobefrin lasts longer than that of epinephrine, but does not endure as long as
that of ephedrine.
Barger and Dale pointed out that the maximal pressor activity of epinephrine and allied
compounds was dependent on the introduction of hydroxyl groups on the para and meta
positions in the basic benzene ring. Ephedrine does not have these hydroxyl groups,
which probably accounts for the fact that it has less vasopressor activity.
The presence or absence of vagal reflexes during the studies of the effects of epinephrine
and cobefrin on the blood pressure were not constant in occurrence under any type
of anesthesia. As a rule, neither substance gave evidence of a reflex vagal slowing
with a concomitant decrease in the blood pressure. The advantage which a few clinical
investigators have claimed for cobefrin is that it does not produce reflex vagal slowing
of the heart. This finding was substantiated. The results which were obtained with
commercial epinephrine were comparable with those obtained with cobefrin. Consequently,
the use of cobefrin instead of epinephrine would appear to have no advantage in this
respect. One outstanding and important difference between these closely allied compounds
is that cobefrin is active when administered by mouth while epinephrine is not. Herein
lies the one major difference in the action of these two substances.
Cobefrin was found to be just as effective as epinephrine in stimulating the perfused
isolated heart of the rabbit, and the ability of cobefrin to cause relaxation of a
rhythmically contracting uterus of a virgin guinea pig or to relieve bronchospasm
was identical with that of epinephrine. To determine the site of destruction of cobefrin
in the body, the Starling heart-lung, heart-lung-liver, and heart-lunghindlimb perfusion
preparations were employed. It was found that practically none of the cobefrin was
inactivated in the heart-lung perfusion experiments, which fact coincides directly
with the results of Elliott's experiments with epinephrine. However, the heart-lung-liver
and the heart-lung-hindlimb perfusion experiments indicated definitely that any large
capillary bed, with the exception of that of the lungs, serves as a site for the elimination
of cobefrin. The liver is by no means as specific an organ for the inactivation of
cobefrin as it is for the inactivation of nicotine or novocain. Studies on the blood
sugar of dogs showed that epinephrine and cobefrin were equally potent in producing
definite increases in the values for the blood sugar, provided the animals were in
a proper state of nutrition.
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Article info
Publication history
Received:
October 23,
1936
Identification
Copyright
© 1937 Published by Elsevier Inc.
