Role of the salivary glands in protecting the stomach against ethanol.
The submandibular gland complex was removed from young adult Wistar rats. Sham operations were performed on control animals. Three weeks later, the animals were starved for 24 hr and after pyloric ligation the stomachs were instilled with 30% ethanol. Two hours later, the animals were killed and the surface areas of the ulcerated mucosae were measured and the values used as ulcer index scores. In male, but not female, rats prior sialoadenectomy significantly exacerbated ethanol-induced gastric ulceration of the glandular stomach mucosa. This increase in ulceration was accompanied by an increase in the backflux of acid into the injured tissue. Sialoadenectomy had no statistically significant effect on histamine-stimulated gastric acid and pepsin secretion when these were measured 3 weeks later. Epidermal growth factor (EGF) was administered subcutaneously to intact animals in which the stomachs had been filled with 30% ethanol. When administered at a dose of 10 micrograms/kg per hr. EGF significantly reduced the ethanol-induced ulceration. High molecular weight nerve growth factor (7S NGF) was administered intragastrically prior to instilling ethanol in the stomachs of intact rats. The NGF had no effect on the severity of ethanol-induced ulcers. These data suggest that saliva protects the gastric mucosa from ethanol-induced ulceration and that salivary EGF is a possible candidate for this protection.
D000818:Animals; D000431:Ethanol / Q000633:toxicity*; D005744:Gastric Acid / Q000378:metabolism; D005753:Gastric Mucosa / Q000378:metabolism; D006632:Histamine / Q000494:pharmacology; D010434:Pepsin A / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D012463:Saliva / Q000502:physiology*; D013276:Stomach Ulcer / Q000139:chemically induced*; D013361:Sublingual Gland / Q000502:physiology; D013363:Submandibular Gland / Q000502:physiology
D000431:Ethanol; D006632:Histamine; D010434:Pepsin A