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Biomedical subjects

D Andersen

Publications and source records attributed to D Andersen.

At least 55 records · Page 3Linked to original sources
PubMed1985

Effect of somatostatin on bethanechol-stimulated gastric pepsin secretion in gastric fistula dogs.

The effect of somatostatin on pepsin secretion was determined in six dogs with gastric fistulas during stimulation with bethanechol. Somatostatin inhibited dose-dependently the stimulated pepsin secretion, with a dose of 0.3 micrograms/kg/h being 35% inhibitory during stimulation with bethanechol, 80 micrograms/kg/h. Continuous infusion of somatostatin for 3 h did not cause any signs of tachyphylaxis. Withdrawal of somatostatin produced a return to the control level. The dose-response kinetics with five doses of bethanechol with and without somatostatin showed inhibition of a noncompetitive type. The effects of somatostatin were not altered by using adrenergic, dopaminergic, or serotonergic blocking drugs.

Adrenergic beta-Antagonists↗
PubMed1985

Effect of somatostatin on bethanechol-stimulated gastric acid secretion and gastric antral motility in dogs with gastric fistula.

The purpose of the present study was to evaluate the effect of somatostatin on gastric acid secretion and gastric antral motility in conscious dogs with gastric fistula. Infusion of bethanechol stimulated dose-dependently acid secretion, whereas the frequency and strength of antral motility was maintained at a high level. Somatostatin inhibited dose-dependently the stimulated acid secretion, whereas the effect on antral motility was more complex, acting especially on the amplitude of the contractions. The effects of somatostatin were not altered by using alpha-adrenergic, beta-adrenergic, dopaminergic, and serotonergic blocking drugs. The dose-response kinetics with four doses of bethanechol with and without somatostatin showed inhibition of a non-competitive type for gastric acid secretion and of a competitive type for antral motility with regard to amplitude.

Adrenergic alpha-Antagonists↗
PubMed1985

Prevention of ulcer recurrence--medical vs surgical treatment. The surgeon's view.

The need for surgical intervention in duodenal ulcer disease will undoubtedly decrease in the years to come. Occasional failure of medical treatment and persistent doubts about the long-term safety of anti-ulcer drugs will continue to make operation the treatment of choice for some patients, however. Long-term medical treatment and surgery can be considered equally acceptable options for most patients. When operation is considered necessary, parietal cell vagotomy fits the requirements of a modern surgical method better than other techniques. The effective medical treatment now available makes postoperative recurrence of ulcer less important than before and lack of postoperative symptoms has replaced fear of recurrent ulceration as the main concern in the value judgement of both doctors and patients.

Cimetidine↗
PubMed1984

A transplantable rat Leydig cell tumor--1. LH and prolactin receptors and effects of the endocrine status of the host animal.

We have examined the binding capacity and properties (affinity, specificity) of LH and prolactin (Prl) receptors in a transplantable rat Leydig cell tumor (H-540) grown in intact, castrated and hypophysectomized rats. LH receptors in adult rat testis and Prl receptors in the rat ventral prostate were examined simultaneously for comparison. The results can be summarized as follows: The qualitative properties (affinity, specificity) of LH and Prl receptors in tumor Leydig cells appear to be identical to those of corresponding receptors in non-tumor tissues. The levels of LH receptors in tumor Leydig cells are only some 1% of that present in normal Leydig cells from adult rats. Tumor Leydig cells grown in hypophysectomized rats had even lower levels of LH receptors; ca. 1/3 of that found in tumors from intact rats. The levels of Prl receptors in the tumor Leydig cells are almost as high as in normal Leydig cells from adult rats. In tumors grown in hypophysectomized rats, the levels of Prl receptors were much lower (ca. 20%) than in tumors from intact or castrated rats. There were great variations in the number of LH and Prl receptors in individual tumors, and there was a positive correlation (r = 0.88; P less than 0.01) between LH and Prl receptors in individual tumors. No differentiation toward a "LH receptor tumor" or "Prl receptor tumor" was observed. Thus, receptors for LH and Prl in tumor cells are qualitatively normal, but the number is greatly (LH) or moderately (Prl) reduced. These receptors in the tumor Leydig cells are stimulated by pituitary hormones.

Animals↗
PubMed1984

Testicular gonadotropin receptors, testicular testosterone, dihydrotestosterone and androstenedione in the developing bull.

The testis homogenate from Red bull (3-17 months of age) show specific binding of hLH and hFSH with Kd of 1.3 +/- 0.1 X 10(-10)M and 1.5 +/- 0.1 X 10(-9)M, respectively. Prepubertal bulls (3-5 3/4 months) exhibit the highest binding capacity of both LH and FSH, revealing the fact that LH and FSH receptors are present in high concentrations prior to the first rise in plasma T. The testicular T concentration was significantly higher in the four prepubertal bulls than in the four older animals in spite of the fact that circulating T is lower before puberty. Thus, local androgen effects within the testis may occur before peripheral androgenization. The prepubertal bull Leydig cell also displayed steroidogenic capacity. The ratio of biologically active (testosterone, dihydrotestosterone) to inactive androgens (androstenedione) increased as the animals approached puberty. Such qualitative changes in steroid production may be one of the factors responsible for peripheral androgenization.

Androgens↗
PubMed1984

Adrenergic receptors and gastric secretion in dogs. Is a "tonic balance" relationship between vagal and beta 2-adrenergic activity a possibility?

The relative influence of adrenergic receptors on gastric acid secretion in the dog stomach with different vagal activity or "tone" is almost unknown. beta-adrenoceptors seem to be most important for the direct effect of adrenergic stimulation on acid secretion. In this study the effects of vagotomy and beta 2-adrenoceptor activity were studied in conscious gastric fistula dogs. Pentagastrin stimulated acid output was increased slightly in non-vagotomized dogs and to its prevagotomy level in vagotomized dogs after propranolol infusion. Practolol showed no such effect. Histamine stimulated acid secretion was not influenced significantly by beta-blockade. Similar dose-response curves were found for non-vagotomized dogs with high beta 2-adrenergic tone and dogs with low vagal tone (vagotomy) after pentagastrin and histamine stimulated acid secretion. This study indicates that a counterbalance between beta 2-adrenergic and cholinergic vagal tone exists. A "tonic balance theory" is suggested and is probably involved in the resulting acid secretion after vagotomy.

Adrenergic beta-Antagonists↗
PubMed1984

Adrenergic influence on pentagastrin and bethanechol stimulated gastric acid secretion in dogs with gastric fistula.

The purpose of this study was to elucidate the effect of alpha-, beta- and dopaminergic receptor stimulation and blockade on pentagastrin and bethanechol stimulated gastric acid secretion in conscious dogs with gastric fistula. Gastric acid secretion was found to be subject to a dose related inhibition by isoprenaline. The dose of isoprenaline producing approximately 50% inhibition was higher in the bethanechol--than the pentagastrin experiments (0.10 vs. 0.03 micrograms/kg/min.) and slightly lower after parietal cell vagotomy. The antisecretory effect was mediated via the beta 1-receptors alone. The inhibitory effect of isoprenaline on pentagastrin stimulated acid secretion showed the characteristics of competitive type and on bethanechol stimulated acid secretion of non competitive type. An increasing and dose-dependent stimulation of bethanechol stimulated gastric acid secretion was found for dopamine 1, 5 and 10 micrograms/kg/min. Dopamine (40 micrograms/kg/min.) exerted an inhibitory effect on pentagastrin and bethanechol stimulated gastric acid secretion mediated, via the beta 1-receptors. The stimulatory effect of low doses of dopamine during bethanechol stimulation could not be defined as an effect via beta-receptors. This dual response, the weak inhibitory effects and the potent decreasing effect on antral gastric motility indicate that dopamine has no physiologic relevant effect on gastric acid secretion. One may conclude that beta 1- and beta 2-receptors may exert an influence on gastric acid secretion in dogs. The main effect of dopamine seems to be on gastric motility, while the effect on gastric acid secretion is of minor importance.

Adrenergic beta-Agonists↗
PubMed1984

Adrenergic influence on gastric mucosal blood flow in gastric fistula dogs.

The aim of this study was to examine the influence of alpha-, beta- and dopaminergic receptors on gastric mucosal blood flow during "high", "normal", and "low" vagal conditions obtained by stimulation with bethanechol and pentagastrin and by parietal cell vagotomy respectively. During pentagastrin and bethanechol stimulation, a linear relationship between gastric acid secretion and mucosal blood flow was observed. During pentagastrin stimulation, dopamine (40 micrograms/kg/min) did not change the blood flow values while a decrease in acid secretion was found. During bethanechol stimulation dopamine (10 micrograms/kg/min) induced an increase in mucosal blood flow and a similar increase in acid secretion. If the dopamine infusion was preceded by alpha-receptor blockade, a pronounced increase in mucosal blood flow was observed without a similar increase in acid secretion. beta-adrenergic stimulation (isoprenaline) reduced the pentagastrin and bethanechol stimulated gastric acid secretion without a similar decrease in mucosal blood flow. beta-blockade (propranolol) increased the pentagastrin stimulated gastric acid secretion in parietal cell vagotomized dogs. This increase in acid output was preceded by an initial increase in mucosal blood flow and in the last two periods a decrease in blood flow. alpha-Blockade (phentolamine) reduced the pentagastrin stimulated gastric acid secretion and gastric mucosal blood flow but the ratio between blood flow and acid secretion was increased, indicating a relatively increasing effect on mucosal blood flow. One may conclude that blood flow and acid secretion are not unconditionally linked and that at least two different mechanisms are involved in blood flow changes in the stomach.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Dopaminergic and beta-adrenergic effects on gastric antral motility.

Stimulation of splanchnic nerves and application of adrenergic drugs have been shown to give variable effects on gastric motor activity depending especially on the background activity. beta-adrenoceptors and dopaminergic receptors mediate inhibitory effect on proximal gastric motor activity. The purpose of the present study was to evaluate the effects of isoprenaline, a beta 1- and beta 2-agonist, and dopamine on gastric antral motility in gastric fistula dogs. Dopamine was used alone and in conjunction with selective blockade of adrenergic and dopaminergic receptors during infusion of bethanechol or pentagastrin inducing motor activity patterns as in the phase III of the MMC and the digestive state respectively. The stimulated antral motility was dose-dependently inhibited by dopamine. The effect was significantly blocked by specifically acting dopaminergic blockers, while alpha- and beta-adrenergic blockers were without any significant effects. Dose-response experiments with bethanechol and dopamine showed inhibition of a non-competitive type. Isoprenaline was used alone and in conjunction with selective blockade of beta 1- and beta 2-receptors during infusion of bethanechol which induces a pattern similar to phase III in the migrating myoelectric complex. The stimulated antral motility was dose-dependently inhibited by isoprenaline. The effect could be significantly blocked by propranolol (beta 1 + beta 2-adrenoceptor blocker) and by using in conjunction the beta 1-adrenoceptor blocker practolol and the beta 2-adrenoceptor blocker H 35/25. The dose-response experiments showed inhibition of a non-competitive type. These studies indicate that gastric antral motility is inhibited by isoprenaline through both beta 1- and beta 2-receptors and by dopamine through specific dopaminergic receptors.

Adrenergic beta-Agonists↗
PubMed1984

Effect of somatostatin on pentagastrin-stimulated gastric acid secretion and gastric antral motility in dogs with gastric fistula.

The purpose of the present study was to evaluate the effect of somatostatin on gastric acid secretion and gastric antral motility in conscious dogs with gastric fistula. Infusion of pentagastrin induced motility with a digestive pattern. Somatostatin inhibited dose-dependently the stimulated acid secretion, whereas the effect on antral motility was more complex, acting especially on the amplitude of the contractions. The effects of somatostatin were not altered by using alpha- and beta-adrenergic, dopaminergic, and serotonergic blocking drugs. The dose-response kinetics with seven doses of pentagastrin with and without somatostatin showed inhibition of a competitive type for gastric acid secretion and of a non-competitive type for antral motility with regard to amplitude.

Adrenergic alpha-Antagonists↗
PubMed1984

Adrenergic receptors and gastric acid secretion in dogs. The influence of beta 2-receptors.

The action of adrenergic subtypes of receptors in gastric acid secretion is still uncertain. The purpose of this study was to establish the influence of beta 2-adrenoceptors in the regulation of gastric secretion in conscious gastric fistula dogs. A dose-related inhibitory effect of beta 2-adrenergic stimulation on gastric acid secretion was found. The rank order of this inhibition was: Pentagastrin greater than bethanechol greater than histamine stimulated acid output. The strong beta 2-adrenergic induced inhibition found for pentagastrin and bethanechol stimulated acid output followed the characteristics of a non-competitive mechanism, while the weaker inhibition of histamine induced acid output seemed to follow a competitive mechanism. The inhibitory effect was not mediated through a decreased gastrin release. Dopamine receptor blockade was found to be without any influence on the inhibitory effect of beta 2-adrenoceptors. It is concluded that beta 2-adrenoceptors inhibit gastric acid secretion through an effect on gastric mucosa. A working hypothesis involving an endogenous inhibitory substance is proposed.

Animals↗
PubMed1983

Plasma catecholamine and serum gastrin concentrations during sham feeding.

Plasma adrenaline, plasma noradrenaline and serum gastrin concentrations were measured before and after sham feeding in eight patients with duodenal ulcer and in four normal subjects. No significant change in the concentrations was observed after sham feeding. In three patients with duodenal ulcer an insulin test resulted in a 25-fold rise in plasma adrenaline. The ulcer patients showed significantly higher levels of plasma adrenaline and plasma noradrenaline than the normal subjects both before and after sham feeding, and this difference was probably not caused only by age difference in the two groups. It is concluded that sympathetic nervous activity and serum gastrin concentrations are not influenced by sham feeding in contrast to the influence of insulin hypoglycemia.

Adult↗