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Biomedical subjects

K Bech

Publications and source records attributed to K Bech.

At least 109 records · Page 6Linked to original sources
PubMed1982

In vitro lymphocyte proliferation in response to polyclonal activators and microbial antigens, and production of immunoglobulins stimulating thyroid adenylate cyclase in Graves' disease.

Cultures of blood lymphocytes from 16 patients with Graves' disease (GD) and 14 matched controls were studied. Incorporation of [14C]thymidine was significantly increased in unstimulated cultures of GD lymphocytes, while the incorporation after stimulation with polyclonal activators (concanavalin A, pokeweed mitogen, phytohaemagglutinin), microbial antigens (E. coli, Candida albicans extract, purified protein derivative of tuberculin, Yersinia enterocolitica serotype 3) and subcellular fractions of human thyroid antigens did not differ from the controls. Due to the increased incorporation in unstimulated cultures, stimulation index is not suitable as an indicator of lymphocyte sensitization. After polyclonal activation or stimulation with thyroid antigens the lymphocytes were cultured for up to 21 days, and the supernatants were investigated for thyroid adenylate cyclase stimulating immunoglobulins (TACSI). No TACSI were demonstrated in supernatants of the lymphocyte cultures neither afer polyclonal activation nor after specific stimulation with several thyroid antigens.

Adenylyl Cyclases↗
PubMed1982

Evidence of a correlation between thyrotrophin receptor binding inhibition and thyroid adenylate cyclase activation by immunoglobulins in Graves' disease before and during long-term antithyroid treatment.

In the present study we have measured in parallel thyrotrophin binding inhibiting immunoglobulins (TBII) and thyroid adenylate cylase stimulating immunoglobulins (TACSI) in patients with Graves' disease (GD) both before and during long-term antithyroid treatment. A statistical model based on the calculation of the differences (TACSI-TBII) is presented, comparing the changes in this parameter to the analytical variation. The correlation between TBII and TACSI in 52 patients with GD before treatment was: r = 0.58, P less than 0.0001. During long-term antithyroid treatment of GD the 2 activities changed in parallel in 39 of 45 patients followed. In a few patients discrepancies were observed, and 1 patient, initially TACSI positive, developed adenylate cyclase inhibiting IgG during treatment but without detectable TBII. In conclusion, 1) TBII and TACSI are significantly correlated in patients with GD both before and during long-term antithyroid treatment, 2) in some patients discrepancies between TBII and TACSI suggest, that these IgGs are heterogeneous with varying capacity for stimulation of the adenylate cyclase and receptor binding, and 3) adenylate cyclase inhibitory IgG without TBII activity was demonstrated in GD.

Adenylyl Cyclases↗
PubMed1982

Effect of dopamine on pentagastrin-stimulated gastric acid secretion and mucosal blood flow in dogs with gastric fistula.

The purpose of this study was to elucidate the effect of intravenously administered dopamine on dopamine receptors and adrenergic receptors in terms of its effect on gastric acid secretion, the kinetic mechanism, blood flow, and antral motility. Dopamine was used alone and in conjunction with selective blockade of alpha-, beta-, and dopaminergic receptors. A significant inhibition of gastric acid secretion was found with the highest dose of dopamine used (40 micrograms/kg/min). The kinetic study showed characteristics of a non-competitive type. The anti-secretory effect dopamine was significantly blocked by non-selective beta-blockade or by selective beta-blockade but not by alpha- or dopaminergic receptor blockade. This suggests that the inhibitory effect of dopamine on gastric secretion is mediated by beta-receptors. There was no significant effect on gastric mucosal blood flow, but the ratio between blood flow and acid secretion was significantly elevated during dopamine infusion, indicating that the acid inhibition was not secondary to changes in blood flow. It is concluded that the dopamine inhibition of acid secretion is mediated by beta 1-receptors, unlike the effect on antral gastric motility, which is mediated by dopamine receptors.

Adrenergic alpha-Antagonists↗
PubMed1982

Effect of dopamine on pentagastrin-stimulated gastric antral motility in dogs with gastric fistula.

The purpose of the present study was to evaluate the effect of dopamine on gastric antral motility in conscious dogs with gastric fistula by using miniature strain-gauge transducers. Infusion of pentagastrin changed the contractile activity to a digestive state. Dopamine, an endogenous catecholamine, was used alone and in conjunction with selective blockade or adrenergic and dopaminergic receptors. The stimulated antral motility was inhibited by dopamine. The effect was significantly blocked by the peripherally acting dopaminergic blocker domperidone and by cis-flupenthixol, which blocks both peripheral and central dopaminergic receptors. The effect of dopamine was not significantly altered by the beta 1-adrenoceptor blocker practolol, the alpha-adrenoceptor blocker phentolamine, or the alpha + beta-adrenoceptor blocker labetalol. Consequently, this study indicates that dopamine acts on gastric antral motility through dopaminergic receptors. beta-Adrenergic receptors, which are active in the impairment of gastric acid secretion, seem not to be involved in the motility response.

Adrenergic alpha-Antagonists↗
PubMed1982

Effect of isoprenaline on bethanechol-stimulated gastric acid secrtion and mucosal blood flow in dogs with gastric fistula.

The prupose of this study was to elucidate the effect of the beta-adrenoceptor stimulation by isoprenaline on cholinergic-stimulated gastric acid secretion and mucosal blood flow in conscious dogs with gastric fistula. Isoprenaline, a beta 1- and beta 2-agonist, was used alone and in conjunction with selective blockade of beta 2 and beta 1 receptors. A low dose of isoprenaline had no significant effect, whereas higher doses had a significant antisecretory effect. The antisecretory effect was significantly blocked by the beta 1-adrenoceptor blocker practolol but not by H 35/25, a beta 2-adrenoceptor blocker. The dose-response curve with five doses of bethanechol with and without isoprenaline was in accordance with a non-competitive inhibition. There was no significant effect on gastric mucosal blood flow, indicating that the acid inhibition was not secondary to changes in blood flow. The inhibitory effect of isoprenaline seems to be mediated by the beta 1 receptors and with an action primarily on the 'gastrinergic receptors'.

Adrenergic beta-Antagonists↗
PubMed1982

Effect of dopamine on bethanechol-stimulated gastric mucosal blood flow and gastric acid secretion in dogs with gastric fistula.

The aim of the present study was to investigate the effect of Dopamine on bethanechol-stimulated gastric acid secretion and mucosal blood flow. dopamine was used alone and in conjunction with selective blockade of the alpha, beta, and dopaminergic receptors. An increasing and dose-dependent stimulation of gastric acid secretion was found for dopamine at 1, 5, and 10 micrograms/kg/min. A significant inhibition of gastric acid secretion was found with the highest dose of dopamine (40 micrograms/kg/min). the stimulatory effect seems to be mediated by more than one receptor, whereas the inhibition by high dopamine doses could be explained by a beta 1 stimulation. Dopamine (10 micrograms/kg/min) was found to increase the bethanechol-stimulated gastric mucosal blood flow. Phentolamine (alpha blackade) increased this dopamine-elevated blood flow further, with a significant increase in the ratio between blood flow and acid secretion, indicating a primary action of the alpha receptors on blood flow. Bethanechol stimulated the gastric acid secretion and blood flow in a parallel manner. It is concluded that alpha-receptor stimulation is the predominant directly acting factor in the regulation of gastric mucosal blood flow, whereas stimulation of beta, muscarinic, and 'gastrinergic' receptors mainly occurs indirectly via changes in parietal cell function. The main effect of dopamine seems to be on gastric motility, whereas the effect on gastric acid secretion is of minor importance.

Animals↗
PubMed1982

Effect of isoprenaline on bethanechol-stimulated gastric antral motility in dogs with gastric fistula.

The purpose of the present study was to evaluate the effect of isoprenaline on gastric antral motility in conscious dogs with gastric fistula, using intraluminal strain-gauge transducers. Infusion of bethanechol increased the motility for both frequency and strength. Isoprenaline, a beta 1- and beta 2-agonist, was used alone and in conjunction with selective blockade of beta 1 and beta 2 receptors. The stimulated antral motility was dose-dependently inhibited by isoprenaline. The effect was significantly blocked by the beta 1 + beta 2-adrenoceptor blocker propranolol and by using in conjunction the beta 1-adrenoceptor blocker practolol and the beta 2-adrenoceptor blocker H 35/25. H 35/25 and particularly practolol reduced the effect of isoprenaline to some extent, but the reduction was not of statistical significance. This indicates that isoprenaline acts on antral motility through both beta 2 and beta 1 receptors. Dose-response experiments with five logarithmically increasing doses of bethanechol and one dose of isoprenaline showed inhibition of a non-competitive type.

Adrenergic beta-Antagonists↗
PubMed1982

Effect of dopamine on bethanechol-stimulated gastric antral motility in dogs with gastric fistula.

The purpose of the present study was to evaluate the effect of dopamine on gastric antral motility in conscious dogs with gastric fistula, using intraluminal strain-gauge transducers. Infusion of bethanechol increased the motility with regard to both frequency and strength. Dopamine, an endogenous catecholamine, was used alone and in conjunction with selective blockade of adrenergic and dopaminergic receptors. The stimulated antral motility was dose-dependently inhibited by dopamine. The effect was significantly blocked by the peripherally acting dopaminergic blocker domperidone. The alpha-adrenoceptor blocker phentolamine reduced the effect of dopamine to some extent, but the reduction was not of statistical significance. The dopamine-inhibited motility was not altered by the beta 1-adrenoceptor blocker practolol or the beta 1 + beta 2-adrenoceptor blocker propranolol. This indicates that dopamine acts on gastric antral motility predominantly through dopaminergic receptors. beta-Adrenergic receptors, which are active in the impairment of gastric acid secretion, do not seem to be involved in the motility response. Dose-response investigations with five increasing doses of bethanechol and one dose of dopamine showed inhibition of a non-competitive type.

Adrenergic alpha-Antagonists↗
PubMed1981

Release of prostaglandin E2 into gastric juice during stimulation of muscarinic- and gastrin receptors in dogs and in humans.

To investigate the causal relationship, if any, between gastric PG formation and gastric acid output, the release of PGE2 into gastric juice has been studied in eight beagle dogs with a gastric fistula, using sustained half-maximal stimulation by bethanechol and pentagastrin, and in eight duodenal ulcer patients, using the combined sham feeding/pentagastrin test. Immunoreactive PGE2 was determined by a method validated by gas chromatography-mass spectrometry and PGE2 values were normalized by expressing them as ng PGE2 released per meq H+ secreted. In the dogs "steady state" PGE2 output (0.4-10 ng/meq H+) was interrupted during continuous i.v. pentagastrin infusion by symmetrical peaks (50-60 minutes of duration) with a maximum of 24 +/- 3.1 ng/meq H+ (mean +/- SEM). During bethanechol stimulation the rhythmic variations were smaller, but the median values for the periods 30 to 180 or 240 minutes significantly (p less than 0.01) higher (3.9-46 ng/meq H+) than in pentagastrin experiments (0.8-20 ng/meq H+). In humans the peak PGE2 output during sham feeding (3.4-41 ng/meq H+) was significantly (p less than 0.02) larger than following bolus stimulation (6/micrograms/kg) by pentagastrin (2.2-18 ng/Meq H+). The findings are consistent with the hypothesis that activation of muscarinic receptors represents the physiologic mechanism by which gastric release of PGs is regulated. Cyclic variations in gastric PG formation appear to occur in response to vagal stimulation since the peaks in PGE2 output were preceded by increased myoelectrical activity (i.e. mean contractile index).

Adult↗
PubMed1981

Serum prolactin and thyrotropin responses to thyrotropin-releasing hormone in men with alcoholic cirrhosis.

The serum concentrations of prolactin (PRL) and thyrotropin (TSH) in 12 males with alcoholic cirrhosis during basal condition and after stimulation with thyrotropin-releasing hormone (TRH) were compared with the concentrations in ten thiazide-treated hypertensive and nine normal men. The basal as well as the TRH-stimulated increase in serum PRL was significantly elevated in the cirrhotic males, while the increase in serum TSH was unchanged, compared with hypertensive and normal men. No correlation between clinical or laboratory parameters and serum PRL was found. Serum estradiol was equal in cirrhotic and control subjects and no correlation was found between serum PRL and serum estradiol. These findings favour the concept that raised serum PRL in cirrhotic patients might be caused by a diminished dopaminergic neurotransmission.

Adult↗
PubMed1981

Influence of thyroglobulin on basal and stimulated human thyroid adenylate cyclase activity.

The interaction of thyroglobulin (Tg), thyroid-stimulating immunoglobulins (TSI), and TSH on human thyroid plasma membranes from nontoxic goiter was studied in vitro by an adenylate cyclase assay system using human thyroid homogenate. Purified Tg [3 X 10(-10) M (0.2 micrograms/ml) to 3 X 10(-8) M (20 micrograms/ml)] exerted a dose- and time-dependent inhibitory influence on basal adenylate cyclase activity. The inhibition was prevented by preincubation with Tg antibody in excess. Tg (3 X 10(-8) M) caused a significant reduction in the TSH- and TSI-stimulated adenylate cyclase activities, but did not influence stimulation with NaF (8 mM). Fractions of thyroid homogenates were obtained by differential centrifugation, and the maximal inhibitory influence of Tg was located in the 5000 X g fraction. Thus, Tg is an efficient inhibitor of basal and TSH- or TSI- stimulated adenylate cyclase activities, and might be involved in a short loop counterregulation of thyroid adenylate cyclase sensitivity in vivo.

Adenylyl Cyclase Inhibitors↗
PubMed1981

Effect of isoprenaline on pentagastrin-stimulated gastric acid secretion in dogs with gastric fistula.

The purpose of this study was to elucidate the effect of a beta 1-adrenoceptor agonist on gastric acid secretion in conscious dogs with gastric fistula. Isoprenaline, a beta 1- and beta 2-agonist was used alone and in conjunction with selective blockade of beta 2- and beta 1-receptors. Isoprenaline dose-dependently inhibited the secretory volume and the acidity. The antisecretory effect of isoprenaline was significantly blocked by the beta 1-adrenoceptor blocker practolol and by the beta 1 + beta 2-adrenoceptor blocker propranolol but not by H 35/25, a beta 2-adrenoceptor blocker. This indicates that isoprenaline acts on the acid secretion exclusively through beta 1-receptors. Dose-response experiments with five logarithmically increased doses of pentagastrin and one dose of isoprenaline showed unchanged calculated maximum response and an increase in half-maximum acid response. It is concluded that the inhibitory effect of isoprenaline on gastric acid secretion is of competitive or uncompetitive type.

Adrenergic beta-Antagonists↗
PubMed1980

Influence of treatment with radioiodine and propylthiouracil on thyroid stimulating immunoglobulins in Graves' disease.

Thyroid stimulating immunoglobulins (TSAb) were measured in fifty-four patients with Graves' disease before treatment with either radioiodine (seventeen patients) or propylthiouracil (PTU) (thirty-seven patients), and followed during treatment. After radioiodine TSAb increased to levels exceeding pretreatment values, and became detectable in three of six originally TSAb negative patients. In most patients TSAb decreased during treatment with PTU, and became undetectable after a mean of 12 months in patients above 40 years, and after a mean of 6 months in patients below 40 years. In order to eliminate the presumed causative agent in Graves' disease, antithyroid treatment should be at least 18 months in patients above 40 years, and at least 12 months in patients below 40 years of age. In twenty-nine patients TSAb were measured at cessation of 2 years antithyroid drug therapy. Ten patients were TSAb positive and all except one relapsed. Five of nineteen TSAb negative patients relapsed. Although TSAb positivity predict relapse, it is not an ideal index of prognosis after antithyroid therapy.

Adult↗
PubMed1980

An improved co-precipitation assay for determination of thyroglobulin antibodies.

A radioassay for determination of thyroglobulin antibodies in human serum using [125I]thyroglobulin co-precipitated with antihuman IgG is described. Serial dilutions of the antibody containing sera gave nearly rectilinear and parallel logit-log curves in conditions of moderate antigen excess. A secondary standard serum calibrated against the Medical Research Council Research standard A 65/93, which by definition c;ntains 1 Mega unit/1 (MU/1) was used for standardization. The mean imprecision in the concentration range 0.74-241 MU/1 was CV = 3% (within assay) and CV = 8% (total). The detection limit was 0.002 MU/1. The assay was compared to an antigen binding capacity method with an imprecision of 15% (total) and a detection limit of 0.1 MU/1. The coefficient of correlation between the two methods was: R = 0.997 (our method = 0.019 x antigen binding capacity -0.33). Based on this 1 Mega unit was found equivalent to 53 nmol thyroglobulin.

Antibodies↗
PubMed1979

TSH and thyroid stimulating antibodies (TSAb) activate thyroid adenylate cyclase through different pathways.

Adenylate cyclase activity in human thyroid homogenates was studied after stimulation with thyrotropin (TSH) and thyroid stimulating antibodies (TSAb). The results show: 1) TSAb prepared from different patients with Graves' disease show different adenylate cyclase activation patterns and a lag phase is frequently observed. 2) TSH and TSAb appear to cause mutually inhibitory activation of thyroid adenylate cyclase. 3] The maximal adenylate cyclase activation is higher with TSH than with TSAb, but this could possibly be due to contamination of TSAb preparations with an adenylate cyclase inhibitor. 4) There is no absolute copurification of TSH sensitive and TSAb sensitive adenylate cyclase in various subcellular fractions of thyroid homogenate. 5) Incubation of thyroid homogenate with cortisol cause a dose dependent decrease in the adenylate cyclase response to TSAb whereas the response to TSH is either increased or unchanged. The results indicate that TSH and TSAb activate thyroid adenylate cyclase through different pathways in the plasma membrane.

Adenylyl Cyclases↗
PubMed1979

Thyroid adenylate cyclase stimulating immunoglobulins in thyroid diseases.

The occurrence of serum immunoglobulins with capacity to stimulate thyroid adenylate cyclase (TSAb) was studied in seventy-two healthy volunteers and 120 unselected patients with various thyroid diseases. A high frequency of TSAb (82.5%, P less than 0.00006) was found in Graves' disease, while TSAb was present only in 13--20% of serum from patients with nontoxic nodular goitre, nontoxic diffuse goitre, toxic adenoma, toxic nodular goitre and myxoedema. These patients had low level of TSAb compared to patients with Graves' disease. In patients with Graves' disease there was no correlation between the level of TSAb and hormonal status except serum triiodothyronine (rs = 0.29, P less than 0.05), and no relation with eye involvement or presence of microsomal thyroid antibodies was found. The results indicate that the human thyroid adenylate cyclase assay system with 1 hour incubation periods is a sensitive method for detection of immunoglobulins with TSH-like capacity to stimulate the thyroid gland.

Adenoma↗