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  • 1
    Electronic Resource
    Electronic Resource
    The role of gastric histamine release in the acid secretory response to pentagastrin and methacholine in the dog (1995)
    Springer
    Inflammation research 44 (1995), S. 327-334 
    Details
    ISSN: 1420-908X
    Keywords: Histamine ; Gastric ; Pentagastrin ; Acid secretion ; Canine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have previously demonstrated that both pentagastrin and methacholine can stimulate histamine release from the canine stomach during short term administration of the secretagogues into the gastrosplenic artery. In this study we tested the hypothesis that gastric histamine release determines the acid secretory response to acid secretagogues. Increasing doses of pentagastrin (2, 6, and 20 ng/kg/min) and methacholine (0.1, 0.3, and 1µg/min) were infused into the gastro-splenic artery in dogs, while gastric acid output, histamine and Nτ-methyl histamine secretory rates were monitored. Histamine and Nτ-methyl histamine concentrations in plasma were measured using GC/NICI-MS. Increasing doses of pentagastrin resulted in increasing gastric output. Total histamine secretory rate expressed as the sum of histamine and Nτ-methyl histamine secretory rate showed a significant increase above basal with the two highest doses of pentagastrin. Regression analysis correlating the dose of pentagastrin to gastric acid output gave a correlation coefficient of 0.586 which was very significant. Regression analysis correlating the total histamine secretory rate to acid output gave a correlation coefficient of 0.498 which was also very significant. Increasing doses of methacholine also resulted in a dose-dependent increase in acid output. Histamine secretory rates showed a statistically significant increase above basal only at the 1µg/min infusion rate, however, the total histamine secretory rates (histamine + Nτ-methyl histamine) were no longer significant at any of the doses of methacholine. Regression analysis correlating the dose of methacholine to gastric acid output gave a correlation coefficient of 0.571 which was significant, while correlating the histamine secretory rate to acid output gave a correlation coefficient of 0.338, not significant, which decreased to 0.079 when the total histamine secretory rates were correlated to acid output. Sixty-eight min infusions of pentagastrin demonstrated a dose-dependent, pulse-like but persistent increase in histamine secretory rate above basal, while long-term infusion of methacholine gave a flat, low-grade histamine stimulation. These data suggest that for pentagastrin, both the dose of pentagastrin and the amount of histamine released determine the acid secretory response with this secretagogue, but the dose of pentagastrin correlates more strongly with acid output. During cholinergic stimulated acid output, only the dose of methacholine correlates with acid output. Thus, for cholinergic stimulated gastric acid output, histamine is not likely to be a final mediator, but for gastrin both its direct action at the parietal cell and the amount of histamine released appear to contribute to the acid secretory response.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01796263
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  • 2
    Electronic Resource
    Electronic Resource
    Effect of somatostatin, secretin, and glucagon on secretagogue stimulated aminopyrine uptake in isolated canine parietal cells (1983)
    Springer
    Inflammation research 13 (1983), S. 265-268 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Somatostatin, secretin, and glucagon have been shown to inhibit gastric acid secretionin vivo and thus have been postulated to act directly on the parietal cell. To test the hypothesis that these peptides directly influence the acid secretory cells, we studied the effect of the three gastrointestinal hormones using aminopyrine uptake as an index of acid production. The parietal cells were stimulated to increase aminopyrine uptake by submaximal concentrations of histamine (10−6 mol/l), methacholine (10−6 mol/l), and pentagastrin (10−6 mol/l), but in no concentrations did these gastrointestinal hormones affect any of the secretagogues' response. Our data suggest that gastrointestinal peptides do not modulate acid secretion at the parietal cell level.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01971476
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  • 3
    Electronic Resource
    Electronic Resource
    Neither dapsone hydroxylation nor cortisol 6β-hydroxylation detects the inhibition of CYP3A4 by HIV-1 protease inhibitors (1998)
    Springer
    European journal of clinical pharmacology 54 (1998), S. 741-747 
    Details
    ISSN: 1432-1041
    Keywords: Key words CYP3A4 ; Dapsone N-hydroxylation ; Cortisol β-hydroxylation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract Objective: This study examined the use of dapsone N-hydroxylation and cortisol 6β-hydroxylation, well accepted in vivo probes of cytochrome P4503A4 (CYP3A4) activity, on defining the effect of three HIV protease inhibitors on CYP3A4 activity. Methods: Subjects from University Hospital Infectious Disease Clinic about to be started on indinavir, and subjects from two clinical studies, one using ritonavir and the other using amprenavir, were recruited to participate in the study. Subjects received dapsone 100 mg p.o. followed by an 8-h urine collection for dapsone, dapsone N-hydroxylamine, cortisol, and 6β-hydroxycortisol concentrations before HIV protease inhibitor administration, and 3–4 weeks into receiving HIV protease inhibitors. Results: None of the HIV protease inhibitors demonstrated statistically significant alterations in dapsone recovery ratio and 6β-hydroxycortisol/cortisol ratio. In fact, with ritonavir, the dapsone recovery ratio tended to increase rather than decrease, suggesting induction. These negative results were found despite evidence of CYP3A4 inhibition by these three HIV protease inhibitors via published drug-drug interactions with drugs that are substrates for CYP3A4. Conclusions: These in vivo assays used to probe CYP3A4 activity are suboptimal, most likely because of the presence of extrahepatic sites of metabolism for both dapsone and cortisol, and multiple CYP isozymes involved in dapsone N-hydroxylation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002280050545
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  • 4
    Electronic Resource
    Electronic Resource
    The effect of aging on the pharmacokinetics and pharmacodynamics of prazosin (1996)
    Springer
    European journal of clinical pharmacology 50 (1996), S. 41-46 
    Details
    ISSN: 1432-1041
    Keywords: Key words Prazosin ; Elderly; pharmacokinetics ; age-related ; pharmacodynamics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract. Objective: The effect of age on the pharmacokinetics and pharmacodynamics of prazosin (α1 adrenoceptor blocker) was studied in 20 healthy volunteers. Patients: Ten elderly (61–81 y) and ten young (23–28 y) subjects were studied. All subjects received 1 mg of prazosin orally in a fasting state. Serial blood samples were collected for calculation of oral pharmacokinetics, and blood pressure and pulse rate were measured during blood collection. Subjects remained supine and fasting for the first three hours post drug administration, after which they were allowed to ambulate and eat. Results: The oral pharmacokinetics of prazosin were not different in the two age groups. The serum t1/2 in the elderly was 210 min while in the young group was 139 min. The AUC0−∞ in the two groups was not different. The Cmax was identical in the two groups, and the time to Cmax was 84 min in the elderly and 114 min in the young subjects. Protein binding was 93.4% in the elderly and 93.5% in the young subjects and the serum α1 acid glycoprotein concentration was not different in the two groups of subjects. Even though the pharmacokinetics of prazosin were unchanged by age, the haemodynamic effects of the drug were greater in the elderly. The fall in systolic blood pressure and mean blood pressure was significantly greater in the elderly group at multiple time points after drug administration while the change in diastolic blood pressure was equivalent in the two age groups. Despite a greater decrease in mean blood pressure in the elderly, the compensatory increase in heart rate was similar in the two age groups suggesting a difference in the baroreceptor reflex in the two age groups. Conclusion: The results of this study demonstrate that age does not alter the pharmacokinetics of oral prazosin, but the pharmacodynamic response at equivalent plasma prazosin concentration is greater in the elderly.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002280050067
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  • 5
    Electronic Resource
    Electronic Resource
    Beta-Adrenergic Blocking Drugs (1985)
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Medicine 36 (1985), S. 145-164 
    Details
    ISSN: 0066-4219
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1146/annurev.me.36.020185.001045
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  • 6
    Electronic Resource
    Electronic Resource
    Histamine-1 receptors do not directly modulate canine gastric acid secretion (1982)
    Springer
    Inflammation research 12 (1982), S. 259-262 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The role of histamine-1 receptors in modulating gastric acid secretion was evaluated in anesthetized dogs with gastric fistulas. Histamine receptor agonists were infused directly into the gastric artery supplying the fundus to avoid any systemic hemodynamic effects. Two experimental approaches were taken to try to determine whether histamine-1 receptors participate in the control of acid secretion. Firstly, we measured the effect of the H1-receptor antagonist, hydroxyzine dihydrochloride, on histamine and dimaprit stimulated acid secretion. Secondly, we measured the effect of H1-receptor agonist on dimaprit stimulated gastric secretion. Although H1-receptor antagonist enhanced stimulated gastric acid secretion to histamine, the antagonist also enhanced stimulated gastric acid secretion to dimaprit (H2-agonist), suggesting that the enhanced gastric acid secretion after administration of H1-receptor antagonist is not because of the inhibition of histamine receptor at the gastric fundus. In addition, 2 doses of H1-receptor agonist infused into the gastric fundus had no effect on dimaprit stimulated gastric acid secretion. These data suggest that H1-receptors do not modulate gastric acid secretion at the level of the gastric fundus in the dog.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01965385
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  • 7
    Electronic Resource
    Electronic Resource
    Histamine-1 receptors do not directly modulate canine gastric acid secretion (1981)
    Springer
    Inflammation research 11 (1981), S. 663-666 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The role of histamine-1 receptors in modulating gastric acid secretion was evaluated in anesthetized dogs with gastric fistulas. Histamine receptor agonists were infused directly into the gastric artery supplying the fundus to avoid any systemic hemodynamic effects. Two experimental approaches were taken to try to determine whether histamine-1 receptors participate in the control of acid secretion. Firstly, we measured the effect of H1-receptor antagonist, hydroxyzine dihydrochloride, on histamine and dimaprit stimulated acid secretion. Secondly, we measured the effect of H1-receptor agonist on dimaprit stimulated gastric secretion. Although H1-receptor antagonist enhanced stimulated gastric acid secretion to histamine, the antagonist also enhanced stimulated gastric acid secretion to dimaprit (H2-agonist), suggesting that the enhanced gastric acid secretion after administration of H1-receptor antagonist is not becacuse of the inhibition of histamine receptor at the gastric fundus. In addition, two doses of H1-receptor agonist infused into the gastric fundus had no effect on dimaprit stimulated gastric acid secretion. These data suggest that H1-receptors do not modulate gastric acid secretion at the level of the gastric fundus in the dog.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01978786
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