Pathogenesis of adrenaline collapse

Abstract

This is a study of the pathogenesis of adrenaline collapse. Up -to now no other theory concerning- the mechanism of its production has been put forward other than that of Bülbring and Burn who attributed it to the blocking action, which the high concentration of adrenaline has upon the synapsis of sympathetic ganglia, the hypotension being due to a vasodilation of sympathetic inhibition origin.

Later experiments of Jiménez Vargas, and Monche who made introcisternal injections of potassium, proved the non-existence of this block. Erlanger and Gasser also, described a certain tendency to vasoconstriction coexisting with the post adrenalinic hypotension: this in contradiction to the theory above exposed.

The authors find a relation between adrenalin-collapse and metabolic disorders ischaemic tissue. In order to prove this conception the authors demonstrate that there is less relationship between the collapse and the absolute dose of adrenaline than between it and the persistence of the drug’s action. A dose of adrenaline is more toxic administered slowly over an hour than in five minutes.

A fall in the alkaline reserve during the collapse is described. The authors find that veritol administered in a sufficient dose can produce collapse with identical action on the alkaline reserve. In small doses, it does not produce shock but has a similar effect.