The fundamental physiological mechanism of anaphylaxis.

Abstract

The following is our conception of the fundamental physiological mechanism of canine anaphylaxis, and constitutes our present working hypothesis with other animal species.

We assume that the capillary endothelium is the initial point of anaphylactic attack and defense. We further assume that in dogs the different capillary systems have different susceptibilities to the anaphylactic insult, the capillaries of the liver having the greatest susceptibility.

On intravenous injection of the usual doses of specific foreign protein into sensitized dogs, the hepatic endothelium alone is unable to resist the anaphylactic insult. There is a sudden increase in capillary permeability in this organ, with the rapid passage of foreign protein and altered blood plasma into the hepatic tissue spaces.

The hepatic parenchyma, in consequence, is immediately thrown into exaggerated, possibly atypical functional activity. The chemical products from this activity pass rapidly into the circulating blood, on account of the increased hepatic capillary permeability. These products, acting in conjunction with the circulating foreign protein and altered blood plasma, break down the endothelial defenses in the extra-hepatic tissues, with the resulting rapid passage of atypical products intor the extra-hepatic tissue spaces.

This conception, we believe, fully accounts for the clinical picture of canine anaphylaxis. Thus, the suddenly increased local tissue pressure from hepatic edema with the resulting passive narrowing of the hepatic capillaries, coupled with the suddenly increased local blood viscosity from plasma loss, would account for the characteristic hepatic stasis. The suddenly reduced available blood volume from hepatic stasis and resulting gastro-intestinal passive congestion, coupled with the reduced blood volume from hepatic and extra-hepatic plasma losses, would account for the characteristic fall in arterial blood pressure.