J.Jpn. Surg. Soc.. 55(7): 728-730, 1954

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Others

A Consideration of the Roles of the Adrenal Cortex and Stress
in the Pathogenesis of Peptic Ulcer

Confirming works by H. Shay et al., typical ulcers can be produced rapidly and uniformly in pylorus-ligated rats. Analysis of gastric contents and cytological studies on gastricgland indicate that the secretion auguments quantitatively and qualitatively in the Shay rat. Ulceration occurs regularly in 48 hour fasted animals, but rather unusual in 24 hour fasted ones, the former group showing more increased activity of the gastric gland and the adrenal cortex. ACTH markedly promotes secretion of HCI and pepsin and ulceration is easy to be produced ; cortisone promotes the secretion slightly, but not ulceration. ACTH stimulates the adrenal cortex to outpour cortical steroids, which act directly upon gastric gland, because its effects are inhibited after adrenectomy, but not after vagotomy or atropinization. The adrenal cortex contributes to maintain neuroglandular function of the vagus nerve at an optimum level, in view of the fact that the stimulation with choline or insulin shock fails to elicit a gastric response, but elicits the response after cortisone substitution in adrenectomized rats with intact vagus innervation. Adrenectomy, and vagotomy as well profoundly reduce gastric secretion and hold ulceration in abeyance. Adrenectomy plus vagotomy reduce gastric secretion still more. In adrenectomized Shay rats, cortisone administration raises gastric secretion up to control level, while incidences of ulceration are retained to lower leval. Various stressor promote gastric secretion and ulceration and somewhat hyperaemia and erosion in the glandular part of the stomach in the Shay rat. However, gastrointestinal ulcers referred to by Selye during G.A.S., occur more reapily followinig adrenectomy, and are remarkably situated in the glandular part of the stomach and not in the cavity, where ulceration in the Shay rat is predominantly seen. Accordingly, it may naturally be concluded that both ligation and fasting induce gastric hypersecretion through nervous and humoral mechanisms concurring and completing each other and at the same time, the above-mentioned discrepancy between gastric secretion and ulceration argues against the acid theory of peptic ulcer. In favar of the vascular theory is vascular involvement of the stomach, which is suggested by the localization of ulcers alongside the course of a blood vessel of the stomach and histological findings showing vasodilatation, stasis, neutrophilic margination, thrombosis and haemorrhage. Indeed vascular lesions may probably supervene secondarily to distension of gastric wall by accumulated gastric contents in later period, vascular lesions in earlier period following ligation identified as vasoconstriction in the intact rat and a marked tendency to stasis in adrenectomized rats, particularly up on exposure to stressor. Because of differences in vascular distribution, mucosa structure and its susceptibility to hyperactive gastric juice and the glandular part of the stomach in the rat, the ulcer is attributable to vasoconstriction and hyperactive gastric juice, while the ulcer in the glandular part is chiefly dependent on vascular lesions alone. As summary, vascular lesions are considered the principial contributing factor in the genesis of peptic ulcer, while hyperactive gastric juice is an ancillary one, though very important, because a devitalized area caused by the former must exist before digestion by the latter can occur. The mechanism of the vasoconstriction needs further studies.
(author's abstract)

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