Measurement of plasma gastrin level by radioimmunoassay in various clinical entities

1972 ◽  
Vol 7 (3-4) ◽  
pp. 295-295
Author(s):  
S. Yamagata ◽  
A. Ishimori ◽  
A. Ohneda ◽  
T. Takebe ◽  
H. Sakurada ◽  
...  
1976 ◽  
Vol 230 (3) ◽  
pp. 784-789 ◽  
Author(s):  
KY Lee ◽  
HH Tai ◽  
WY Chey

In five conscious dogs with gastric fistula and two duodenal cannulas, plasma RIA secretin and gastrin levels were determined in response to 1) infusion of 0.1 N HCl in the proximal duodenal cannula, 2) ingestion of a meal, and 3) intraduodenal infusion of 0.1 N HCl following ingestion of a meal. Significant increases in plasma RIA secretin levels occurred during duodenal acidification. However, no significant change occurred in the secretin levels after ingestion of a meal, whereas significant increase in plasma gastrin level was observed. Postprandial duodenal pH remained above 4.5 for 3 h.


1998 ◽  
Vol 69 (10) ◽  
pp. 955-959
Author(s):  
Yasuhiko NISHIGUCHI ◽  
Madoka SUTOH ◽  
Akio TAKENAKA ◽  
Hiroshi SATO

Digestion ◽  
1982 ◽  
Vol 23 (4) ◽  
pp. 245-252 ◽  
Author(s):  
A. Bosshard ◽  
D. Pansu ◽  
J.A. Chayvialle ◽  
A. Reinberg

2000 ◽  
Vol 118 (4) ◽  
pp. A513
Author(s):  
Grzegorz Bombski ◽  
Daria Orszulak-Michalak ◽  
Beata Neneman ◽  
Ewa Malecka-Panas

1995 ◽  
Vol 269 (5) ◽  
pp. G699-G705 ◽  
Author(s):  
A. Nishida ◽  
A. Kobayashi-Uchida ◽  
S. Akuzawa ◽  
Y. Takinami ◽  
T. Shishido ◽  
...  

Female rats were treated orally for 13 wk with YM022 (300 mumol.kg-1.day-1) and with omeprazole (400 mumol.kg-1.day-1) or famotidine (900 mumol.kg-1.day-1) with or without YM022. At 2 h after the last dose, YM022 and omeprazole markedly inhibited basal and pentagastrin-induced acid secretion. Famotidine was less potent than YM022 and omeprazole against both secretions. The degree of increase in plasma gastrin level in the three groups was parallel to the antisecretory potencies of the drugs. At 14 days after the cessation of omeprazole treatment, the secretory response to pentagastrin increased above that of the control. This hyperresponse lasted for > or = 56 days. In the famotidine-treated group, a small increase in secretory response to pentagastrin was observed but was not statistically significant. The increase in secretory response to pentagastrin was paralleled by an increase in mucosal cell mass. In contrast, YM022 not only exhibited a long-lasting inhibition of pentagastrin-induced acid secretion but also prevented the hyperresponse to pentagastrin caused by omeprazole. These results indicate that the hypergastrinemia caused by long-term administration of antisecretory drugs increases mucosal secretory response to pentagastrin through a gastrin/cholecystokinin B receptor-mediated pathway in rats.


Parasitology ◽  
1981 ◽  
Vol 82 (3) ◽  
pp. 401-410 ◽  
Author(s):  
N. Anderson ◽  
J. Hansky ◽  
D. A. Titchens

SUMMARYRadio-immunoassay of plasma gastrin showed that hypergastrinaemia developed in sheep during experimental infections with Ostertagia circumcincta. Elevations of plasma gastrin occurred within 8 days of the first dose of infective larvae, with the most marked increase being after 11–20 days when adult worms would be expected to be present in the abomasum. Increases of plasma gastrin levels from 69·0 ± 7·6, 28·7 ± 5·3, 48·7 ± 5·9 and 60·6 ± 9·4 pg/ml before infection to maxima of 650, 230, 900 and 750 pg/ml respectively were recorded in 4 sheep infected for the first time. In 2 others which had been previously infected and then treated with anthelmintic, plasma gastrin rose from 16·0 ± 4·0 and 377 ± 87 pg/ml to maxima of 260 and 900 pg/ml at 24 and 29 days after re-infection, respectively. The cause of hypergastrinaemia has not been established. The elevation of abomasal pH which occurs in ostertagiasis may result in increased gastrin levels but is thought not to be the only cause since plasma gastrin increased before the abomasal pH rose and developed in sheep infected for a second time although their abomasal contents remained at pH 4·0 or lower. The presence of the parasite is critical for development of hypergastrinaemia as shown by return of the gastrin level to normal following therapy with an anthelmintic. It was shown that the parasites do not depend on the hypergastrinaemia since O. circumcincta became established in antrectomized sheep in which hypergastrinaemia did not develop.


1986 ◽  
Vol 70 (4) ◽  
pp. 333-338 ◽  
Author(s):  
S. Morimoto ◽  
A. Miyauchi ◽  
K. Fukuo ◽  
S. Imanaka ◽  
H. Yamamoto ◽  
...  

1. The effects of synthetic [Asu1,7]-eel calcitonin (0.5 MRC unit/kg body weight intravenously for 30 min) on circulating levels of human calcitonin, calcium and gastrin were investigated in five patients with medullary carcinoma of the thyroid. 2. Blood samples were obtained before and 15, 30, 60, 90, 120 and 180 min after commencement of infusion of [Asu1,7]-eel calcitonin. Plasma levels of human calcitonin were measured by radioimmunoassay. Cross-reactivity with [Asu1,7]-eel calcitonin in this assay was negligible. 3. On infusion of [Asu1,7]-eel calcitonin, the mean plasma level of human calcitonin decreased significantly to 71.0 ± 8.7% of the basal level (mean ± sem, P < 0.05) after 30 min and 68.4 ± 25.4% of the basal level (P < 0.05) after 60 min. The serum calcium level also decreased significantly, but lagged behind the decrease of human calcitonin, being 95.1 ± 0.7% of the basal level (P < 0.01) at 120 min and 94.8 ± 0.6% of the basal level (P < 0.02) at 180 min. The mean plasma gastrin level did not change significantly on infusion of [Asu1,7]-eel calcitonin. 4. In pooled data for all times, the percentage change in human calcitonin was not significantly correlated with either the percentage change in calcium (r = −0.25, P > 0.1) or the percentage change in gastrin (r = −0.3 8, P > 0.1). 5. These data suggested that [Asu1,7]-eel calcitonin suppressed calcitonin secretion in patients with medullary carcinoma of the thyroid. The mechanism of its effect is unknown.


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