IgE production in two types of genetically different rats.
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Biomedical subjects
Publications and source records attributed to T H Hanahoe.
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Insulin potentiated the dextran anaphylactoid reaction in untreated rats and in rats pretreated with a protein synthesis inhibitor or with a lymphopenic agent. Incubation of rat lymphatic tissue with insulin failed to produce a factor potentiating the histamine-releasing action of dextran when this was studied in both in vivo and in vitro tests. It thus seems that insulin is exerting its potentiating effect on the dextran response through processes not involving synthesis of new protein or interaction with lymphocytes.
Synthetic linear dextran of molecular weight 40,000 produces the systemic anaphylactoid reaction in rats although it is about 4 times less active than the natural branched dextran of similar molecular weight. Similarly, it is less active on local injection into the foot or skin. However, in rats which have been bred for non-reactivity to systemic dextran, it is more active on local injection, resembling the activity of a branched natural dextran of much lower molecular weight (6,000). In human skin, the synthetic linear 40,000 sample is also more active than the natural branched sample of similar molecular weight in producing a wheal and erythema. The results suggest that the dextran receptor in the skin of man may be similar to that in rats genetically resistant to systemic dextran.
Intracutaneous injections of a glucan contaminant of invert sugar solutions and crude cane sugar into human skin produced a localised wheal and erythema reaction. The glucan was also active on intradermal injection into both dextran-sensitive and dextran-resistant rats.
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Low doses of calcium inhibited the local anaphylactoid response of rat paw and skin to dextran.
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