The gastric secretion of pepsin in man TABLE

The control of gastric pepsin secretion continues to excite controversy. The diversity in the results obtained by different investigators may be due, at least in part, to the varying techniques employed to estimate pepsin activity. Thus, edestin (Polland and Bloomfield, 1929), gelatin (Gilman and Cowgill, 1930), egg albumen (Vineberg and Babkin, 1931), beef haemoglobin (Anson and Mirsky, 1932), and human plasma (Hunt, 1948) have each been used as substrates; again, the time of digestion, pH, temperature, and the actual parameters of proteolytic activity have been diverse. There is widespread acceptance of the view that vagal stimulation evokes the secretion of acid gastric juice rich in pepsin. In dogs with innervated gastric pouches, this has been demonstrated by direct stimulation of the vagus nerves in the neck (Browne and Vineberg, 1932; Vineberg, 1933); in man, insulin-induced hypoglycaemia has been used to effect central excitation of the vagus nerves which in turn stimulated a gastric acid and pepsin secretory response (Ihre, 1938; Chinn, Book, and Beams, 1951; Janowitz and Hollander, 1952; Harrower, Brook, and Cooper, 1956). In contrast to our increasing knowledge of the effect of surgical vagotomy on acid secretion by the stomach little is known of its effect on spontaneous pepsin secretion. The results of such a study are reported in the first part of this paper. While histamine is known to be a very potent stimulus of acid gastric secretion, debate continues regarding its effect on the secretion of pepsin. In dogs, Gilman and Cowgill (1930), and Vineberg and Babkin (1931) found that histamine failed to stimulate pepsin secretion; by contrast Bucher and Ivy (1941) concluded from their experiments using repeated doses of histamine that pepsin secretion was slightly increased. In man, Toby (1937) and Ihre (1938) using small doses of histamine concluded that the drug was without a stimulant effect on pepsin cells. On the other hand, Ashford, Heller, and Smart (1949) and Hunt (1960), using slightly larger doses, found histamine to increase pepsin output, Hunt demonstrating a correlation with the acid response. Most observers, finding an increased output of pepsin following histamine stimulation, have attributed this to a 'wash out' of preformed pepsin by the copious flow of watery acid juice (Polland and Bloomfield, 1929; Toby, 1937; Bucher, Grosman, and Ivy, 1945). In the second part of this paper we report the results of a study in which the output of pepsin has been estimated following the administration of histamine in the dosage known to elicit a maximal acid secretory response.