Summary
The results reported here have compelling implications concerning gastric mucosal damage in detecting the mechanism of cinchophen-induced gastric lesions in dogs. The acute type of cinchophen gastric lesion, a condition characterized by bleeding and/or diffuse superficial gastric erosions of the fundic gland area, is indicative of so called “stress ulceration” and may be due to activating intramucosal pepsinogen during a rapid increase in endogenous corticosteroid levels. Exogenously administered large doses of corticosteroid or cinchophen solely explained the existence of the correlation between gastric mucosajuice pepsin ratio (MJPR) and the gastric lesion. The greater the increase in MJPR, the greater the change in fundic glandular mucosal destruction. Thus the diffuse superficial mucosal destruction of the fundic gland area, occurring shortly after the medications, was estimated as intramucosal digestion. On the other hand, the chronic cinchophen ulcer in the antral mucosa would be due to both an increased output of gastric pepsin secretion and a decreased mucous secretion which is caused by continuous relatively high basal levels of the steroids. The importance of the role of corticoids in relation to gastric pepsin secretion was sufficiently estimated from the results of MJPR measurements. These findings provide information on the pathogenesis of two types of cinchophen induced gastric lesions.
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Bollman, J.L., Stalker, L.K. and Mann, F.C.: Experimental peptic ulcer produced by cinchophen. Arch Int. Med., 61: 119–128, 1938.
Simonds, J.P.: Mode of origin of experimental gastric ulcer induced by cinchophen. Arch. Path., 26:44–50, 1938.
Varro, V. and Csernay, L.: Experimental production of peptic ulcer by administration of cinchophen. In: Pathophysiology of Peptic Ulcer, ed. by Skoryna, S.C., McGill University Press, Montreal, pp 281–290, 1963.
4) Nagamachi, Y. : Importance of gastric mucosal pepsin as an etiological background to two types of cinchophen gastric lesions. 5th World Congress of Gastroenterology, Advance Abstracts, Mexico City, pp 183, 1974.
Ishihara, K. and Nagamachi, Y.: Experimental production of chronic peptic ulcer in dogs by hypothalamic implants of cinchophen. Recent Advances in Gastroenterology, Proc. 3rd World Congr. Gastroenterol., 2: 137–141, 1967.
6) Ishihara, K. and Nagamachi, Y. : Hypothalamic control of cinchophen induced gastric lesions. 4th World Congress of Gastroenterology, Advance Abstracts, Copenhagen, pp 25, 1970.
Nagamachi, Y. and Ishihara, K.: Role of the hypothalamus in the pathogenesis of cinchopheninduced gastric ulcers in dogs. Am. J. Dig. Dis., 15: 1083–1089, 1970.
Selye, H.: The sress of life. New York, McGraw-Hill, 1956.
Nagamachi, Y. and Taniguchi, A.: Effect of emotional stress on gastric secretion: Its evaluation in peptic ulcerogenesis. Jap. J. Gastroenterol., 72: 673–683, 1975.
Nagamachi, Y.: Gastric mucosal pepsin as a factor affecting experimentally-induced gastric erosions in dogs. Jap. J. Gastroenterol., 69: 1151–1162, 1972.
Bucher, G.R., Grossman, M.I. and Ivy, A.C.: A pepsin method: The role of dilution in the determination of peptic activity. Gastroenterology, 5: 501–511, 1945.
Mattingly, D.: A simple fluorimetric method for estimation of free 11 -hydroxycorticoids in human plasma. J. Clin. Path., 15: 329–336, 1962.
Menguy, R. and Masters, Y.F.: Effect of cortisone on mucoprotein secretion by gastric antrum of dogs: Pathogenesis of steroid ulcers. Surgery, 54: 19–28, 1963.
Nakamura, S.: Effects of cinchophen on gastric mucous secretion in antral pouch dogs. Kitakanto Med.J., 19: 105–111, 1969.
Nagamachi, Y.: Effect of solcoseryl on gastric mucosal microcirculation and gastric secretion: Inhibitory effect of solcoseryl on cinchophen ulcer production. J. New Remedies & Clinics, 24: 1850–1859, 1975.
Nagamachi, Y.: Changes in the antral mucosal pepsin in dogs with chronic ulcer: Pathogenesis of cinchophen ulcer. Gastroenterol. Jap., 2: 320–327, 1976.
Max, M. and Menguy, R.: Influence of adrenocorticotropin, cortisone, aspirin, and phenylbutazone on the rate of exfoliation and the rate of renewal of gastric mucosal cells. Gastroenterology, 58: 329–336, 1970.
Nagamachi, Y.: Experimental gastric ulcer and central nervous system with special reference to the ulcer etiology by central nervous system. Clin. Physiol., 2: 357–371, 1972.
Nagamachi, Y.: Cinchophen ulcer. In: Experimental Gastric Ulcer: Pathological model and its pathogenesis, Japan Medical Center Press, eds. by Umehara, S. et al., Tokyo, pp 119–129, 1976.
20) Nagamachi, Y. : New way of inducing cinchophen ulcer in the dog: Some studies on its pathogenesis. In: Progress in Peptic Ulcer, Akadémiai Kiadó, eds. by Mózsik, Gy. and Jávo, T., Budapest, pp. 553–567, 1976.
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Nagamachi, Y. Significance of gastric mucosal pepsinogen and plasma corticosteroid levels in the course of cinchophen ulceration. Gastroenterol Jpn 12, 13–20 (1977). https://doi.org/10.1007/BF02773997
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DOI: https://doi.org/10.1007/BF02773997