Relationship of Stress-Induced Histidine Decarboxylase to Circulatory Homeostasis and Shock

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Abstract
Histidine decarboxylase activity of mouse tissues is increased by stress and by injection of epinephrine and norepinephrine, suggesting a balance between histamine and catechol amines producing a component of circulatory homeostasis. Imbalance during intense stress might lead to failure of circulatory homeostasis and to shock. Reasons for discounting histamine as "shock toxin" may be invalid.