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Distribution and Properties of Anaphylactic and Venom-Induced Slow-Reacting-Substance and Histamine in Guinea Pigs¹

From the Department of Medicine, College of Physicians and Surgeons, Columbia University

Abstract

A striking parallel between the capacity of specific antigen and cobra venom to give rise to slow-reacting-substance activity in tissues of sensitized guinea pigs was demonstrated. By either method of treatment lung was the major source of slow-reacting-substance. Aorta, ileum, spleen and uterus showed considerably less capacity to form slow-reacting-substance. Antigen and venom showed significant differences in their ability to cause histamine release from various tissues. Both materials caused histamine release from lung, but venom produced considerably more histamine release than antigen from heart, kidney and diaphragm.

Of several tissue lipid extracts examined, only lung lipid extract produced SRS on treatment with venom. Typical SRS activity was found to be present in untreated lipid extracts of brain and small intestine.

Histamine was found in lipid extracts of lung and was dialyzable.

Anaphylactic SRS was not dialyzable until it had been extracted into 80% ethanol in water. SRS formed from chopped lung treated with venom, however, was found to be dialyzable without extraction into ethanol. On the other hand, SRS prepared from lung lipid extract treated with venom was not dialyzable before or after ethanol extraction.

The distribution of ethanol extracted anaphylactic SRS between ether and water at different pH values showed that it was not completely extractable into ether even at pH 2 to 3. Gasliquid chromatography of anaphylactic SRS preparations following methanolysis did not show a pattern of fatty acids different from control samples. On the basis of these observations anaphylactic SRS does not appear to be a fatty acid.

Four metabolites of histamine, N-acetylhistamine, imidazole-acetic acid, methylhistamine and methylimidazole-acetic acid, as well as histamine incubated with venom, failed to show SRS activity.

Footnotes

¹ Supported in part by grants from the National Institute of Allergy and Infectious Diseases (AI 01578), the National Heart Institute (H-2907), the American Heart Association and the Health Research Council of the City of New York (U-1235).