Abstract

1. 1. In view of present experiments, the immunologic property of antisera to induce passive cutaneous sensitization to guinea pig skin is attributed to the guinea pig smooth-muscle-sensitizing antibody, not conditioned by presence of precipitins. The human-skin-sensitizing antisera property (of human or animal origin) is neither related to the muscle-sensitizing property nor responsible for the induction of passive sensitization of guinea pig skin (PCA). 2. 2. The fixation of antibody responsible for passive cutaneous reactivity is dependent upon competitive fixation of reactive antibody gamma globulin and serum gamma globulin. The ratio of antibody to serum globulin seems to determine the degree of saturation of the skin receptors with reactive and nonreactive gamma globulin. 3. 3. The efficacy of antihistamine, heparin, and hydrocortisone to inhibit passive cutaneous anaphylaxis in guinea pig is limited. Administration of increased doses does not promote increased inhibition. Nontoxic doses of adrenaline are the most effective. The vasoconstricting effect of adrenaline appears to emphasize the vasodilation as an important partial mechanism in passive cutaneous anaphylaxis. 4. 4. Passive cutaneous anaphylaxis in the guinea pig is a manifestation of an interaction between a passively fixed antibody and circulating antigen simultaneously at all points of sensitivity. It is a vascular phenomenon with dominant venous and capillary manifestations, rather than an arteriolar response as in Arthus phenomena. This is evidenced by the macroscopic observations and the microscopic findings in passive cutaneous anaphylaxis.

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