Experimental gastric carcinogenesis in the rat. Effects of hypergastrinemia and acid secretion

Clifford Deveney, Hugh Freeman, Lawrence W. Way

Research output: Contribution to journalArticle

40 Citations (Scopus)

Abstract

The present experiments examined in rats the influence of chronic hypergastrinemia and the resulting gastric hyperacidity on induction of gastric adenocarcinoma by N-methyl-N′-nitro-N-nitrosoguanidine (MNNG). Three groups of animals were studied: (A) control rats (no operation, normogastrinemia); (B) rats with antrectomy and Billroth II (normogastrinemia); and (C) rats with implantation of the antrum into the colon and Billroth II (hypergastrinemia). All rats were fed MNNG, 83 μg/ml, in drinking water for 6 months and were observed for 6 more months before being killed. The number, location, and histology of malignant gastric neoplasms were recorded. The incidence of tumors in the proximal gastric remnant of the Billroth II antrectomy rats was 88 percent, significantly greater than the incidence in the proximal gastric remnant (excluding the implanted antrum) of Billroth II antral implant rats (50 percent) or in control rats (50 percent). In addition, 19 gastric neoplasms were found in the 12 antra implanted into the transverse colon. Thus antrectomy Billroth II predisposed the animals to tumors, which was at least partially offset by hypergastrinemia. This suggests that gastric mucosa is more vulnerable to carcinogens after antrectomy and Billroth II, and the effects of hypergastrinemia (or acid secretion and mucosal growth) reduce this vulnerability. Hypergastrinemia did not protect the antrum from tumor induction when the antrum was removed from exposure to acid. These data suggest that in rats (1) antrectomy Billroth II predisposes to carcinogenically induced gastric cancer, (2) hypergastrinemia directly or indirectly decreases this predisposition, and (3) in the presence of hypergastrinemia and after removal from the acid stream, the antrum is highly vulnerable to the carcinogenic effects of MNNG.

Original languageEnglish (US)
Pages (from-to)49-54
Number of pages6
JournalThe American Journal of Surgery
Volume139
Issue number1
DOIs
StatePublished - 1980
Externally publishedYes

Fingerprint

Gastroenterostomy
Stomach
Carcinogenesis
Acids
Methylnitronitrosoguanidine
Gastric Stump
Stomach Neoplasms
Neoplasms
Transverse Colon
Incidence
Gastric Mucosa
Drinking Water
Carcinogens
Histology
Colon
Adenocarcinoma
Growth

ASJC Scopus subject areas

  • Surgery

Cite this

Experimental gastric carcinogenesis in the rat. Effects of hypergastrinemia and acid secretion. / Deveney, Clifford; Freeman, Hugh; Way, Lawrence W.

In: The American Journal of Surgery, Vol. 139, No. 1, 1980, p. 49-54.

Research output: Contribution to journalArticle

@article{d3353b0c0de54d13bac3f3f1069f2e41,
title = "Experimental gastric carcinogenesis in the rat. Effects of hypergastrinemia and acid secretion",
abstract = "The present experiments examined in rats the influence of chronic hypergastrinemia and the resulting gastric hyperacidity on induction of gastric adenocarcinoma by N-methyl-N′-nitro-N-nitrosoguanidine (MNNG). Three groups of animals were studied: (A) control rats (no operation, normogastrinemia); (B) rats with antrectomy and Billroth II (normogastrinemia); and (C) rats with implantation of the antrum into the colon and Billroth II (hypergastrinemia). All rats were fed MNNG, 83 μg/ml, in drinking water for 6 months and were observed for 6 more months before being killed. The number, location, and histology of malignant gastric neoplasms were recorded. The incidence of tumors in the proximal gastric remnant of the Billroth II antrectomy rats was 88 percent, significantly greater than the incidence in the proximal gastric remnant (excluding the implanted antrum) of Billroth II antral implant rats (50 percent) or in control rats (50 percent). In addition, 19 gastric neoplasms were found in the 12 antra implanted into the transverse colon. Thus antrectomy Billroth II predisposed the animals to tumors, which was at least partially offset by hypergastrinemia. This suggests that gastric mucosa is more vulnerable to carcinogens after antrectomy and Billroth II, and the effects of hypergastrinemia (or acid secretion and mucosal growth) reduce this vulnerability. Hypergastrinemia did not protect the antrum from tumor induction when the antrum was removed from exposure to acid. These data suggest that in rats (1) antrectomy Billroth II predisposes to carcinogenically induced gastric cancer, (2) hypergastrinemia directly or indirectly decreases this predisposition, and (3) in the presence of hypergastrinemia and after removal from the acid stream, the antrum is highly vulnerable to the carcinogenic effects of MNNG.",
author = "Clifford Deveney and Hugh Freeman and Way, {Lawrence W.}",
year = "1980",
doi = "10.1016/0002-9610(80)90229-9",
language = "English (US)",
volume = "139",
pages = "49--54",
journal = "American Journal of Surgery",
issn = "0002-9610",
publisher = "Elsevier Inc.",
number = "1",

}

TY - JOUR

T1 - Experimental gastric carcinogenesis in the rat. Effects of hypergastrinemia and acid secretion

AU - Deveney, Clifford

AU - Freeman, Hugh

AU - Way, Lawrence W.

PY - 1980

Y1 - 1980

N2 - The present experiments examined in rats the influence of chronic hypergastrinemia and the resulting gastric hyperacidity on induction of gastric adenocarcinoma by N-methyl-N′-nitro-N-nitrosoguanidine (MNNG). Three groups of animals were studied: (A) control rats (no operation, normogastrinemia); (B) rats with antrectomy and Billroth II (normogastrinemia); and (C) rats with implantation of the antrum into the colon and Billroth II (hypergastrinemia). All rats were fed MNNG, 83 μg/ml, in drinking water for 6 months and were observed for 6 more months before being killed. The number, location, and histology of malignant gastric neoplasms were recorded. The incidence of tumors in the proximal gastric remnant of the Billroth II antrectomy rats was 88 percent, significantly greater than the incidence in the proximal gastric remnant (excluding the implanted antrum) of Billroth II antral implant rats (50 percent) or in control rats (50 percent). In addition, 19 gastric neoplasms were found in the 12 antra implanted into the transverse colon. Thus antrectomy Billroth II predisposed the animals to tumors, which was at least partially offset by hypergastrinemia. This suggests that gastric mucosa is more vulnerable to carcinogens after antrectomy and Billroth II, and the effects of hypergastrinemia (or acid secretion and mucosal growth) reduce this vulnerability. Hypergastrinemia did not protect the antrum from tumor induction when the antrum was removed from exposure to acid. These data suggest that in rats (1) antrectomy Billroth II predisposes to carcinogenically induced gastric cancer, (2) hypergastrinemia directly or indirectly decreases this predisposition, and (3) in the presence of hypergastrinemia and after removal from the acid stream, the antrum is highly vulnerable to the carcinogenic effects of MNNG.

AB - The present experiments examined in rats the influence of chronic hypergastrinemia and the resulting gastric hyperacidity on induction of gastric adenocarcinoma by N-methyl-N′-nitro-N-nitrosoguanidine (MNNG). Three groups of animals were studied: (A) control rats (no operation, normogastrinemia); (B) rats with antrectomy and Billroth II (normogastrinemia); and (C) rats with implantation of the antrum into the colon and Billroth II (hypergastrinemia). All rats were fed MNNG, 83 μg/ml, in drinking water for 6 months and were observed for 6 more months before being killed. The number, location, and histology of malignant gastric neoplasms were recorded. The incidence of tumors in the proximal gastric remnant of the Billroth II antrectomy rats was 88 percent, significantly greater than the incidence in the proximal gastric remnant (excluding the implanted antrum) of Billroth II antral implant rats (50 percent) or in control rats (50 percent). In addition, 19 gastric neoplasms were found in the 12 antra implanted into the transverse colon. Thus antrectomy Billroth II predisposed the animals to tumors, which was at least partially offset by hypergastrinemia. This suggests that gastric mucosa is more vulnerable to carcinogens after antrectomy and Billroth II, and the effects of hypergastrinemia (or acid secretion and mucosal growth) reduce this vulnerability. Hypergastrinemia did not protect the antrum from tumor induction when the antrum was removed from exposure to acid. These data suggest that in rats (1) antrectomy Billroth II predisposes to carcinogenically induced gastric cancer, (2) hypergastrinemia directly or indirectly decreases this predisposition, and (3) in the presence of hypergastrinemia and after removal from the acid stream, the antrum is highly vulnerable to the carcinogenic effects of MNNG.

UR - http://www.scopus.com/inward/record.url?scp=0018920613&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0018920613&partnerID=8YFLogxK

U2 - 10.1016/0002-9610(80)90229-9

DO - 10.1016/0002-9610(80)90229-9

M3 - Article

VL - 139

SP - 49

EP - 54

JO - American Journal of Surgery

JF - American Journal of Surgery

SN - 0002-9610

IS - 1

ER -