Transient Increase of Blood Histamine Level Induced by Pentagastrin Continuous Monitoring by in vivo Microdialysis
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Abstract:
Background: Since few studies of (penta)gastrin-induced histamine release from the gastric mucosa into blood has been performed, an effect of pentagastrin on histamine level of rat blood was examined by using the in vivo microdialysis method. Methods: Pentagastrin was perfused through the microdialysis probe implanted into the jugular vein of urethane-anesthetized rats or in urethane-anesthetized, totally gastrectomized rats, and dialysis samples of blood were concurrently collected. Histidine decarboxylase (HDC) activities and histamine contents in the glandular stomach and gastric acid output after pentagastrin stimulation were also investigated. Results: Pentagastrin induced a transient increase of blood histamine in a dose-dependent manner but failed to cause any increase of blood histamine in the totally gastrectomized rat. Pentagastrin also induced increases of the HDC activity in the glandular stomach and of the gastric acid output. The peak histamine level in blood occurred 40 min after pentagastrin perfusion, whereas the peak acid secretion occurred after 80–120 min and then leveled off. Conclusions: The transient increase of blood histamine induced by pentagastrin is attributable to the histamine released from enterochromaffin-like cells and could be monitored by using the in vivo microdialysis method.Keywords:
Pentagastrin
Microdialysis
Histidine decarboxylase
Pentagastrin
Histidine decarboxylase
Cimetidine
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Abstract In Lai-rats gastric mucosal histamine and histidine decarboxylase were estimated after stimulation of gastric acid secretion by intravenous infusions of submaximal doses of pentagastrin for 1 or 2 h. Pentagastrin produced a dose-dependent acid response with a maximum of 26 μ equiv H+ per 10 min at a dose of 2.56 μg kg−1 min−1. There was a linear relation between the log dose of pentagastrin and the activation of gastric histidine decarboxylase. The highest dose of pentagastrin yielded a histidine decarboxylase activity of 200% of the unstimulated level when infused for 1 h and of 290% when infused for 2 h. No reduction of gastric mucosal histamine could be detected whatever the dose of pentagastrin or the duration of infusion. It was concluded (1) that stimulation of gastric histidine decarboxylase is a physiological function of gastrin-like peptides, (2) that a reduction of gastric mucosal histamine by gastrin or pentagastrin is a pharmacological rather than a physiological effect, and (3) that no negative feedback relation exists beween gastric mucosal histamine and the activation of histidine decarboxylase.
Pentagastrin
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Pentagastrin
G cell
Parietal cell
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We have studied the capacity of several mammalian tissues to inactivate synthetic human gastrin I and its synthetic analog, pentagastrin. Slices of each tissue studied were incubated with either gastrin or pentagastrin and the degree of inactivation was determined by both radioimmunoassay and bioassay. The results demonstrate that there is an in vitro potential for the inactivation of gastrin in all the tissues tested. There was a close correlation between the results obtained with radioimmunoassay and those obtained with bioassay.
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Abstract The log dose-response curves for graded doses of the secretagogues porcine gastrin (a partially purified sample; the crude and its gastrin II equivalent), histamine, and a gastrin pentapeptide (pentagastrin) on the perfused stomachs of urethanized rats are parallel. On weight basis, pentagastrin is 60 times and histamine four times more active than the crude porcine gastrin preparation. The partially purified porcine gastrin sample is six times more potent than histamine but half as potent as pentagastrin. On molar basis gastrin (as the pure porcine gastrin II) has 3000 times the activity of histamine dihydrochloride and 5000 times that of the histamine base. Gastrin is 50 times more potent than pentagastrin. Gastrin and pentagastrin are more potent and have less undesirable side-effects than histamine.
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Histidine decarboxylase
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1. A method of gastrin bio‐assay is described which can be used on as little as 30 ng synthetic human gastrin I at a minimum concentration of 2·5 ng/ml. 2. Pentagastrin or synthetic human gastrin I added to cat plasma can be stored on ice or at 4° C, for periods up to 27 hr without apparent loss of gastrin activity. 3. Between 1½ and 13 min after the rapid I.V. injection of pentagastrin in the anaesthetized cat and between 1½ and 15 min after the injection of synthetic human gastrin I, there is a rapid reduction of the gastrin concentration in the arterial plasma. The data relating log 10 gastrin concentration in arterial plasma with time can be fitted by a single term. 4. Studies in vitro show that over the periods of time involved in the in vivo studies, both pentagastrin and synthetic human gastrin I are stable in cat plasma at 37° C in concentrations which occurred in the circulating plasma. 5. The half‐life of pentagastrin in the circulating arterial plasma of the anaesthetized cat is 1·50 min ( S.E. ± 0·08) and the half‐life of synthetic human gastrin I is 2·65 min ( S.E. ± 0·09).
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