The effect on the normal dog heart of expressed tissue juice from hearts of dogs poisoned with diphtheria toxin

The injection of moderately large doses of diphtheria toxins into animals is followed by no change in arterial blood pressure until after the elapse of a certain latent period, varying from 24 hours in the rabbit to 2-4 days in the dog, when it begins to fall. The fall in blood pressure, having once occurred, rapidly proceeds, so that within a very short time the animal is dead (30 minutes in the rabbit). Both vasomotor paralysis and cardiac failure are responsible for the fall, although it is evident that the cardiac failure is the more important as the immediate cause of death, since mere isolation of the vasomotor center — as after spinal transection — is not followed by such rapid cardiac failure. The vasomotor paralysis of course accelerates the cardiac failure. 1

Roily further found that isolation by Hering's method of the heart of a rabbit just dying as a result of diphtheria inoculation and its perfusion with blood from a healthy animal did not in the slightest degree delay the failure.

Although a certain amount of histological change seems always to be present in the myocardium after death from the inoculation of diphtheria toxins, yet it has been considered by Rolly and others as scarcely of sufficient intensity to account for the sudden failure. Furthermore, addition of diphtheria toxins even in very large dosage to the fluid perfused through a Langen-dorff heart preparation does not influence the beat; nor does its perfusion with the blood of a moribund animal (from diphtheria inoculation).

It has been suggested, therefore, (by Rolly, et al.) that the cardiac failure is due to a functional change resulting from the gradual assimilation of toxin by the cardiac muscle until so much had been taken up as to paralyze the muscle. Hence, the long latent period and the rapid course of the failure.