scholarly journals A Novel Method of Measurement of Gastric Acid Secretion in Intact and Conscious Rats

1984 ◽  
Vol 104 (10) ◽  
pp. 1090-1094 ◽  
Author(s):  
MASAKI HAGIWARA ◽  
HIROSHI WATANABE ◽  
KEIKO KAWATA ◽  
KAZUO WATANABE
1995 ◽  
Vol 488 (2) ◽  
pp. 501-508 ◽  
Author(s):  
K Shimizu ◽  
P Li ◽  
K Y Lee ◽  
T M Chang ◽  
W Y Chey

1990 ◽  
Vol 524 (2) ◽  
pp. 208-212 ◽  
Author(s):  
Myung Suk Kim ◽  
Yang Hyeok Jo ◽  
Shin Hee Yoon ◽  
Sang June Hahn ◽  
Duck Joo Rhie ◽  
...  

2002 ◽  
Vol 75 (2) ◽  
pp. 92-97 ◽  
Author(s):  
V. Sibilia ◽  
F. Pagani ◽  
F. Guidobono ◽  
V. Locatelli ◽  
A. Torsello ◽  
...  

1996 ◽  
Vol 270 (1) ◽  
pp. G220-G224 ◽  
Author(s):  
S. Higashide ◽  
G. Gomez ◽  
G. H. Greeley ◽  
C. M. Townsend ◽  
J. C. Thompson

The purpose of this study was to examine whether an intermediate form of amidated gastrin, glycine-extended gastrin (Gly-G), can stimulate gastric acid secretion in conscious rats prepared with gastric fistulas. Intravenous administration of Gly-G (20 nmol.kg-1.h-1) alone for 2 h did not stimulate gastric acid secretion; however, administration of Gly-G (20 nmol.kg-1.h-1) in combination with a bolus administration of gastrin (9.5 nmol/kg) potentiated acid secretion significantly. Gastric acid secretion in response to gastrin alone and gastrin plus Gly-G (2 nmol.kg-1.h-1) was 109.1 +/- 21.6 and 170.1 +/- 27.7 mueq.kg-1.h-1, respectively (P < 0.05). Gastric acid secretion in response to gastrin alone and gastrin plus Gly-G (20 nmol.kg-1.h-1) was 84.8 +/- 17.5 and 164.1 +/- 29.3 mueq.kg-1.h-1, respectively (P < 0.05). Intravenous administration of Gly-G (20 nmol.kg-1.h-1) failed to increase histamine (1 mg/kg)-stimulated acid output. These results demonstrate that Gly-G can selectively potentiate the stimulatory effect of gastrin on acid secretion in rats and that the unprocessed form of gastrin, Gly-G, can exert a biological effect in the stomach.


1999 ◽  
Vol 254 (3) ◽  
pp. 623-627 ◽  
Author(s):  
Nobuhiko Takahashi ◽  
Toshikatsu Okumura ◽  
Hiroto Yamada ◽  
Yutaka Kohgo

1998 ◽  
Vol 275 (1) ◽  
pp. G22-G28 ◽  
Author(s):  
P. Li ◽  
T. M. Chang ◽  
W. Y. Chey

Secretin is an enterogastrone that inhibits gastric acid secretion and motility. Recently, it was reported that secretin inhibited gastric emptying via a capsaicin (Cap)-sensitive vagal afferent pathway. However, a possible role of the sensory afferent pathway in secretin-inhibited acid secretion has not been clarified. We investigated whether or not the acid secretion suppressed by secretin is modulated by a vagal and/or splanchnic afferent pathway in rats. Subdiaphragmatic perivagal (PV) or periceliac ganglionic (PCG) application of Cap (10 mg/ml) or vehicle was performed in both conscious and anesthetized rats 2 wk before experiments. Bilateral vagotomy was performed in some conscious rats 5 days before studies. Pentagastrin was administered intravenously at 0.6 μg ⋅ kg−1 ⋅ h−1. Secretin (20 pmol ⋅ kg−1 ⋅ h−1iv) or 0.03 N HCl (4.32 ml/h id) was infused in conscious rats with gastric cannulas or anesthetized rats with ligation of the pylorus, respectively. A rabbit antisecretin serum was injected in some anesthetized rats before duodenal acidification. Secretin significantly inhibited pentagastrin-stimulated acid secretion by 63% ( P < 0.01), which was abolished by both vagotomy and PV treatment of Cap in conscious rats. In anesthetized rats, duodenal infusion of 0.03 N HCl suppressed pentagastrin-induced acid secretion by 59.4% ( P < 0.01), which was reversed not only by antisecretin serum but also by PV application of Cap. However, PCG treatment with Cap did not influence the inhibition by secretin or duodenal acidification in either awake or anesthetized rats. These results indicate that the inhibition by secretin of pentagastrin-stimulated acid secretion is mediated by a Cap-sensitive vagal afferent pathway but not via a splanchnic afferent pathway in rats.


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