Protection by histamine and metabolites in anaphylaxis, scalds, and endotoxin shock

¹ College of Physicians & Surgeons of Columbia University, First Surgical Division, Bellevue Hospital; and Departments of Physiology and Biochemistry, New York Medical College, Flower and Fifth Avenue Hospitals, New York City

The release of toxic factors has been implicated in the mechanism of shock from various forms of trauma. If histamine (H) released after anaphylaxis, endotoxin shock, or thermal burns is a lethal factor in mice, priming with (H) before injury would presumably enhance mortality. Mice were pretreated with (H) or certain metabolites prior to inducing shock via horse serum anaphylaxis, scald injury, or lethal dose of E. coli endotoxin. Large doses of (H) did not enhance mortality; actually, mortality from these three forms of shock was lowered by pretreatment with (H) or imidazoleacetic acid, but not by other metabolites tested. The data, while unexplained, do not appear to support hypotheses assigning an active role to (H) release in these three forms of shock in mice.