ANGIONEUROTIC EDEMA 283 
those areas whose vasodilators previously have been 
irritable and near fatigue, or whose vasoconstrictors 
have been irritable and respond to stimuli in an exag- 
gerated manner before giving way to fatigue. Under 
such circumstances the formation of a wheal could not 
occur, as no increased permeability of the vessel walls 
has occurred. Where localized vasodilation has pre- 
ceded fatigue, wheal formation may be expected, due 
to localized vessel-wall permeability. Once established, 
whether preceding or following wheal formation, local 
areas of vasoconstriction persist, if undisturbed by 
treatment, until the local vasoconstrictors in turn be- 
come fatigued, when relaxation supervenes and the 
lesion disappears. That the disappearance of the local 
vasoconstriction and wheal is due to fatigue paralysis 
of the local vasoconstricting nerve end-plates would 
seem to be proven by the fact that local anesthesia 
produced by sponging the affected surface lightly with 
chloroform will cause much more rapid disappearance 
of wheals. 
The part played by the posterior lobe of the pituitary 
body in this series of phenomena does not become ap- 
parent in the milder varieties of urticaria, but in the 
severer forms is often plainly evident in the severe 
diarrhea, colic, and other gastrointestinal manifesta- 
tions related to unusual peristaltic action or an ex- 
cessive contractility of the non-striated musculature. 
Vasoconstrictor fatigue necessarily would be swift 
and the disappearance of wheals prompt, were the af- 
fected vasoconstrictors not supported and sustained in 
their contraction by some agency external to them- 
selves. As previously pointed out, that agency in the 
body which possesses this ability to the most marked 
degree, i. e., selective contractile effect upon the muscle 
fibres of the circulatory system, is adrenin, the product 
of the adrenal medulla. It would appear, therefore, 
that long-persisting urticarial wheals, like those of 
