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B Thuesen

Publications and source records attributed to B Thuesen.

30 records · Page 2Linked to original sources

The relationship of secretin and somatostatin levels in plasma to glucose administration and acid secretion during fasting.

The concentrations of secretin and somatostatin in plasma were measured in 10 healthy subjects during a 4-day fast. The fast induced increased concentrations of plasma secretin (from 1.2 +/- 0.5 to 9.5 +/- 2.3 pmol/l) and somatostatin (from 5.2 +/- 1.5 to 8.6 +/- 1.7 pmol/l). Gastric aspiration for 1 h suppressed the high concentrations of secretin by 46% and somatostatin by 27%. The intravenous infusion of glucose reduced the plasma secretin even further by 88%; the decrease in somatostatin was not statistically significant. The study shows that gastric aspiration and/or glucose infusion suppressed the high plasma concentration of secretin and that factors other than hyperchlorhydria must be involved in the hypersecretinemia seen during starvation. The elevated plasma somatostatin concentration seen during starvation may be a consequence of increased acid secretion.

Adult↗

Histaminergic regulation of prolactin secretion: dose-response relationship and possible involvement of the dopaminergic system.

Histamine (HA) may participate in the neuroendocrine regulation of pituitary hormone secretion. HA diphosphate infused iv for 120 min in a dose of 9, 18, 30, or 50 micrograms/kg BW.h to six normal men stimulated PRL secretion in a dose-dependent manner [absolute change in PRL (delta PRL) area = 52 X (HA dose) - 618; r = 0.9926; P less than 0.001]. The stimulatory effect of HA was modest and occurred during the second hour of infusion. This increase might be due to the opposing effects of HA on PRL secretion, specifically stimulation via H1 receptors and inhibition via H2 receptors. The PRL-releasing effect of 11 micrograms HA dihydrochloride was not significantly different from that of an equimolar dose of HA diphosphate (18 micrograms). Selective activation of H2 receptors by combined infusion of HA and the H1 receptor antagonist mepyramine inhibited PRL secretion compared to the effect of NaCl [delta PRL, -55 +/- 23 (+/- SEM) vs. -20 +/- 17 microIU/ml; P less than 0.01; n = 6). Mepyramine infused alone had no effect (delta PRL, -43 +/- 22 vs. -33 +/- 30 microIU/ml; n = 6). Selective activation of H1 receptors by combined infusion of HA and the H2 receptor antagonist cimetidine stimulated PRL secretion (delta PRL, 193 +/- 40 vs. -20 +/- 17 microIU/ml; P less than 0.0005; n = 6). When infused alone, cimetidine had only a modest and late stimulatory effect (delta PRL, 35 +/- 22 vs. -27 +/- 15; P less than 0.025; n = 6). Dopamine receptor blockade with metoclopramide (MET; 10 mg, three times daily, orally) did not prevent the PRL-inhibiting action of H2 receptor activation (delta PRL, -374 +/- 70 vs. -184 +/- 107 microIU/ml; P less than 0.01; n = 6), whereas the PRL-stimulating effect of H1 receptor activation was abolished by the drug (delta PRL, -249 +/- 64 vs. -174 +/- 54 microIU/ml; n = 6). The latter effect of MET was not due to exhaustion of the lactotrophs, since 200 micrograms TRH stimulated PRL secretion during MET treatment. These findings suggest that the H1 receptor-mediated PRL-stimulating effect of HA occurs through an inhibition of the dopaminergic system, whereas the H2 receptor-mediated PRL-inhibiting effect of HA does not involve dopaminergic neurons.

Adult↗

Effect of histamine on basal and TRH/LH-RH-stimulated PRL and LH secretion during different phases of the menstrual cycle in normal women.

The neurotransmitter histamine (HA) may participate in the regulation of some pituitary hormones. We, therefore, investigated the effect of HA (50 micrograms/kg body weight/h, infusion 0-240 min) on basal and thyrotropin-releasing hormone (TRH) and luteinizing hormone releasing hormone (LH-RH) stimulated prolactin (PRL) and LH secretion in 5 normal women during the early follicular and the luteal phases of the same menstrual cycle. HA had no effect on the basal secretion of the two hormones. However, the PRL response to 200 micrograms TRH during the HA infusion was significantly increased compared to the response to a saline control infusion during the early follicular phase (peak responses were 1,902 +/- 398 vs. 1,228 +/- 230 microIU/ml, p less than 0.025) and during the luteal phase (peak responses were 2,261 +/- 335 vs. 1,647 +/- 245 microIU/ml, p less than 0.05). HA potentiated the LH response to 100 micrograms LH-RH during the early follicular phase (peak responses were 37.1 +/- 4.9 vs. 26.9 +/- 4.5 mIU/ml, p less than 0.05) and during the luteal phase (peak responses were 79.3 +/- 22.5 vs. 50.7 +/- 11.4 mIU/ml, p less than 0.025). We, therefore, found HA to have a potentiating effect on TRH/LH-RH-stimulated PRL and LH secretion in women. The results are similar to our previous findings in men, although the potentiating effects of HA were higher in women.

Adult↗

Histamine-induced paradoxical growth hormone response to thyrotropin-releasing hormone in normal men.

GH responses to TRH occur in patients with certain diseases, such as acromegaly, severe liver disease, uremia, and mental disorders, and presumably reflect disruption of normal hypothalamic control of GH secretion. Since histamine (HA) inhibits hypothalamic stimulation of GH secretion, we investigated the combined effect of HA receptor activation and TRH administration on GH secretion in normal men. Eight men were given 4-h infusions of the following: saline, HA, HA plus mepyramine (Me; and H1-antagonist), HA plus cimetidine (C; an H2-antagonist), and C alone. TRH (200 micrograms) was injected iv 2 h after the start of each infusion. HA alone or in combination with either antagonist had no effect on basal or TRH-stimulated TSH secretion and no effect on basal GH secretion. However, when TRH was injected during H1 stimulation by HA plus C, GH secretion increased significantly [from 0.7 +/- 0.1 to 7.1 +/- 1.8 (+/- SEM) ng/ml; P less than 0.01] in seven of eight subjects. This GH response was reproducible and did not occur when saline was administered instead of TRH. A smaller and delayed GH response to TRH occurred during infusions of HA alone (from 0.8 +/- 0.1 to 4.9 +/- 1.0 ng/ml; P less than 0.05). No effect of TRH on GH secretion occurred during the infusion of saline (1.2 +/- 0.3 ng/ml), HA plus Me (0.9 +/- 0.1 ng/ml), or C (2.2 +/- 1.0 ng/ml). There was a significant increase in GH secretion after cessation of the infusions of HA (from 3.4 +/- 1.1 to 7.5 +/- 2.2 ng/ml) and HA plus Me (from 0.8 +/- 0.1 to 5.1 +/- 1.8 ng/ml). This rebound in GH secretion might indicate an inhibitory effect of TRH during H2-receptor stimulation. This concept is supported by the significantly smaller GH response to TRH during HA infusion than during HA plus C infusion (P less than 0.01). The study indicates that H1-receptor stimulation induces a stimulatory effect of TRH on GH secretion in normal men and that H2-receptor stimulation possibly induces an inhibitory effect of TRH on GH secretion.

Adult↗

Chronic obstructive pancreatitis associated with gallstone in a child.

A case of chronic obstructive pancreatitis in a 15-year-old girl is presented. The aetiology of the disease is believed to be due primarily to an impacted gallstone in the ampulla of Vater and secondarily to a large intraductal calculus in the pancreas. A pancreaticogastrostomy was performed and the large pancreatic calculus removed.

Adolescent↗

Histamine regulation of prolactin secretion through H1- and H2-receptors.

Histamine (HA) regulates PRL secretion in the rat by a stimulatory effect through H1-receptors and an inhibitory effect through H2-receptors. The effect of HA antagonists on basal and TRH-stimulated PRL secretion was investigated in five normal men. During saline infusion, serum PRL declined, as seen normally after sleep. HA infusion caused a significantly higher PRL secretion than that observed during the saline infusion [maximum change in PRL (delta PRL), 28 +/- 20 vs. -71 +/- 30 microIU/ml; P less than 0.05]. This effect of HA on PRL secretion was inhibited during the combined infusion of HA and the H1-antagonist mepyramine (delta PRL, 28 +/- 20 vs. -77 +/- 13 microIU/ml; P less than 0.025). The PRL-stimulating effect of HA was strongly enhanced during the combined infusion of HA and the H2-antagonist cimetidine (delta PRL, -28 +/- 20 vs. 132 +/- 57 microIU/ml; P less than 0.0125). This effect of HA and cimetidine on PRL secretion was higher than the effect of cimetidine alone (delta PRL, 132 +/- 57 vs. 17 +/- 22 microIU/ml; P less than 0.05). This shows that the H2-antagonist is not the only stimulator of PRL secretion. During the different infusions, serum PRL concentrations were in the following rank order: mepyramine less than saline less than HA less than cimetidine less than HA plus cimetidine. The same rank order was found for the PRL responses to TRH during the different infusions. These data indicate a HA stimulatory effect through H1-receptors and an inhibitory effect through H2-receptors on PRL secretion in human males.

Cimetidine↗

Comparison between dose-responses of prolactin, thyroid stimulating hormone and growth hormone to two different histamine H-2 receptor antagonists in normal men.

The effects of the histamine H2-receptor antagonists, ranitidine and cimetidine on prolactin (PRL), thyroid stimulating hormone (TSH), and growth hormone (GH) were studied in six normal males. Intravenous bolus injections of saline and of 50, 100, and 200 mg ranitidine and 300 mg cimetidine were tested. Ranitidine (100 and 200 mg) and cimetidine (300 mg) caused a significant increase in PRL secretion, whereas saline and ranitidine (50 mg) did not. TSH and GH secretion were unaffected by all doses. A dose-response relationship between ranitidine and PRL was established, and a dose of 65 mg ranitidine was found to be the minimal effective PRL-releasing dose. Plasma ranitidine concentration was measured by specific RIA. The results indicate an effect of H2-receptor antagonists on physiological functions in the control of PRL secretion. Histamine, therefore, may play a role in the regulation of PRL secretion.

Adult↗