ライフサイエンスコーパス: pentagastrin

1 20 min before and 150 min after the start of pentagastrin.

2 retion stimulated by intravenous infusion of pentagastrin.

3 delivery blocked the facilitatory effects of pentagastrin.

4 taglandin-independent effects of intravenous pentagastrin.

5 received an intravenous bolus of placebo and pentagastrin.

6 er in basal HPA axis activity or response to pentagastrin.

7 Microinjections of the CCK-B agonist, pentagastrin, (0.5 and 1.0 nmol/0.25 microliter) facilit

8 13 (17 nmol/0.25 microliter) 55 min prior to pentagastrin (1.0 nmol/0.25 microliter) delivery blocked

9 Pentagastrin administration induced acid secretion, but

10 ificant difference in AUC and C(max) between pentagastrin and famotidine arms, thereby effectively mi

11 t (BAO) and maximal acid output (MAO) during pentagastrin and insulin-induced hypoglycemia were measu

12 on of the cholecystokinin-B receptor agonist pentagastrin and placebo were evaluated in patients with

13 l motor nucleus reduced the acid response to pentagastrin by 29%.

14 ed dose-dependently the net acid response to pentagastrin by 40.8+/-11.1, 75.4+/-12.8 and 96.7+/-19.4

15 c.) 60 min after the start of an intravenous pentagastrin infusion; gastric acid secretion was monito

16 not ASPTV, decreased MAO (p < 0.05); (after pentagastrin, OPGV from 26.4 +/- 1.7 mEq/hour to 11.3 +/

17 sies, and measurement of peak acid output to pentagastrin (PAO(PG)).

18 act (TE) and synthetic human gastrin-17 I or pentagastrin (PG) were studied.

19 Pentagastrin (PG; 10 microg/kg IV) or saline was then gi

20 This surface acidity was enhanced by pentagastrin (pH 3.5 +/- 0.2) and eliminated by omeprazo

21 (P = .02) and ACTH (P = .01) levels, despite pentagastrin's robust stimulation of both hormones (P<.0

22 ally active as judged by their inhibition of pentagastrin stimulated acid secretion in conscious dogs

23 2.9 and ranged from 1.1 - 8.4 with a median pentagastrin stimulated gastric pH of 1.60 (range 1.0 -

24 Immediately after basal and pentagastrin-stimulated acid and pepsin outputs were mea

25 lasma pharmacokinetics and the inhibition of pentagastrin-stimulated acid output following bolus intr

26 nist in vitro as judged by its inhibition of pentagastrin-stimulated acid secretion in an isolated, l

27 ability and is a potent inhibitor in vivo of pentagastrin-stimulated acid secretion in the rat when d

28 in 14 or the sst2 agonist DC 32-87 inhibited pentagastrin-stimulated acid secretion in wild-type mice

29 , there was a 79.0+/-3.9% peak inhibition of pentagastrin-stimulated acid secretion.

30 nd in the gastric mucosa, inhibits basal and pentagastrin-stimulated acid secretion.

31 te that bombesin acts in the VLRF to inhibit pentagastrin-stimulated gastric acid secretion through s

32 strin and somatostatin immunoreactivity, and pentagastrin-stimulated gastric acid secretion, were sim

33 to exhibit greater subjective sensitivity to pentagastrin than do normal subjects.

34 Patients' exaggerated anxiety responses to pentagastrin were normalized by the intervention.