Abstract

Protection against anaphylactic shock in mice by reserpine has been shown to be a delayed phenomenon, probably not dependent upon a direct effect of reserpine. The release and depletion of catechol amines by reserpine show little likelihood of being responsible for protection because these substances are in themselves protective against anaphylactic shock, while β-TM 10, a drug which interferes with their release is not. Since L-α-methyl dopa and reserpine both deplete serotonin, and since both protect against anaphylactic shock, it is proposed that serotonin depletion is responsible for the protection. Enterochromaffin substance is depleted in anaphylactic shock. It is also depleted by reserpine and serotonin, both of which protect against anaphylactic shock when given prior to challenge with antigen. The amount of enterochromaffin substance seems to correlate with susceptibility to anaphylactic shock. The behavior of animals undergoing anaphylactic shock and the effect of shock on body temperature is similar to the effects on behavior and temperature of treatment with reserpine, which is known to release serotonin. The effect of monoamine oxidase inhibition on animals undergoing anaphylactic shock is also similar to the effect of monoamine oxidase inhibition on animals given reserpine. These results are consistent with the views that the release of serotonin is causally related to anaphylactic shock in mice and that serotonin is accumulated in the chromogenic material of the enterochromaffin cell.