The effect of calomel on plasma epinephrine in the rat and the relationship to mechanisms in pink disease.

Zahorsky (1922) stated that he was inclined to the view that calomel was the causative agent in pink disease. However, some patients were encountered having no history of calomel ingestion, so the idea was dismissed. Lesesne Smith of South Carolina considered that mercury was involved. His belief led Davison (1938) to include mercury as the aetiological agent in the 1938 edition of his current text. Ten years later scientific evidence for the involvement of mercury was furnished by the work of Warkany and Hubbard (1948, 1953) and by Fanconi and Botsztejn (1948). The mode of action of mercury has not been understood, especially by workers investigating the autonomic dysfunction. They have tried to determine the nature of the dysfunction either by indirect physiological studies (Day, Smith and Klingman, 1939; Vulliamy, 1952; Bower, 1954; Farquhar, Crawford and Law, 1956) or by observation of the therapeutic effect of antisympathetic drugs (Gillespie, 1952; Bower, 1954; Peterson and Laughmiller, 1954). Their work supports the contention that excessive action of the sympathetic division exists. This contention is also supported by the findings that basal metabolic rate and venous pressure are increased in pink disease (Cheek, 1957). The methods involved in earlier attempts to measure blood epinephrine in this disease (Cheek, Hetzel and Hine, 1951) are now known to be inadequate. Other work (Cheek and Hicks, 1950; Cheek, 1953) drew attention to the role of 'stress' in pink disease, to the failure of patients to withstand intercurrent infections, atmospheric heat, and intravenous hypotonic solutions, and of further electrolyte loss.