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Biomedical subjects

J Bugajski

Publications and source records attributed to J Bugajski.

At least 73 records · Page 4Linked to original sources
PubMed1984

Interference of clonidine and alpha-methyl-p-tyrosine with stress and central histaminergic stimulation of the corticosterone response in rats.

In conscious rats clonidine given intracerebroventricularly 1 h prior to a mild stress of immobilization intensified the stress-induced increase of pituitary-adrenocortical response, measured indirectly through corticosterone concentration in blood serum. The corticosterone response to clonidine was abolished by i.c.v. pretreatment of rats with yohimbine, an alpha 2-adrenergic antagonist, and was antagonized by pretreatment with phenoxybenzamine, an alpha 1-adrenergic antagonist. Clonidine intensified also the corticosterone response induced in stressed rats by i.c.v. injected histamine, 2-pyridylethylamine (PEA), a H1-receptor agonist, and dimaprit, a H2-receptor agonist. The depletion of brain catecholamines by alpha-methyl-p-tyrosine (alpha-MT) considerably increased the corticosterone response to stress but did not substantially change the response to histamine, PEA and dimaprit in stressed rats. These results suggest that clonidine increases the corticosterone secretion induced by a mild stress and histamine and histamine H1 and H2 agonists mainly through the activation of central alpha 2-adrenoceptors. The increase by alpha-MT of the stress-induced corticosterone response may indicate the inhibitory role of central catecholamines in the pituitary-adrenocortical response to stress in rats.

Adrenergic alpha-Antagonists↗
PubMed1984

Effect of intracerebroventricular impromidine on pituitary-adrenocortical response to stress in rats.

In the rats subjected to a mild stress of immobilization impromidine, and H2-receptor agonist, given 60 min prior to the stress, intensified the stress-induced increase in hypophyseal-adrenocortical response, evaluated indirectly through the corticosterone concentration in the blood serum. Impromidine was far more potent but only about half as efficient as histamine, 4-methyl histamine (4-MH) and dimaprit. The effect of impromidine was abolished by pretreatment of the rats with cimetidine. The alpha-adrenergic blockers phenoxybenzamine, phentolamine and yohimbine, almost totally antagonized the corticosterone response to impromidine in stressed rats. Propranolol, a beta-adrenergic blocker, abolished the corticosterone response to impromidine but did not antagonize the response to 4-MH and dimaprit. The effect of impromidine was not modified by i.c.v. pretreatment of the rats with atropine. The results obtained show that impromidine is far more potent but less efficient than histamine and the previously known selective H2-receptor agonists in inducing the pituitary-adrenocortical response in stressed rats. These results also suggest that impromidine may release norepinephrine but not interact with cholinergic receptors while stimulating the corticosterone response in stressed rats.

Adrenal Cortex↗
PubMed1984

The effect of adrenergic and cholinergic antagonists on central histaminergic stimulation of pituitary-adrenocortical response under stress in rats.

A possible interaction of central histaminergic receptors with adrenergic and cholinergic muscarinic neurons in increasing the pituitary-adrenocortical response under stress, assessed indirectly from the corticosterone concentration in blood serum, was investigated in conscious rats. All the drugs were administered intracerebroventriculary, the antagonists 15 to 30 min prior to the agonists. The histamine-induced increase in serum corticosterone levels of stressed rats was considerably antagonized by prazosin, phenoxybenzamine, phentolamine and yohimbine, alpha 1 and alpha 2-adrenergic antagonists. These antagonists abolished or significantly attenuated the corticosterone response to 2-pyridylethylamine (PEA), an H1-receptor agonist, and to dimaprit and 4-methylhistamine(4-MeHA), H2-receptor agonists. Propranolol, a beta-adrenergic blocker, did not substantially change the corticosterone response induced by histamine or histamine H1- and H2-receptor agonists. Similarly, atropine was ineffective in blocking the increase in serum corticosterone responses induced by either histamine or PEA and dimaprit in stressed rats. These results suggest that both alpha 1- and alpha 2-adrenergic receptors, but not beta-adrenergic and cholinergic muscarinic receptors interact with central H1 and H2 histaminergic stimulation of the increased pituitary-adrenocortical response in stressed rats.

Adrenal Cortex↗
PubMed1984

Effect of intracerebroventricular clonidine on serum corticosterone levels in rats.

In conscious, nonstressed rats clonidine given intracerebroventricularly (i.c.v.) increased the pituitary-adrenocortical response evaluated indirectly from corticosterone concentration. The maximum significant increase occurred 60 min after a dose of 10 micrograms. The alpha 2-adrenoceptor antagonist yohimbine given alone i.c.v. in low doses (0.05-1 microgram) had no effect on plasma corticosterone levels, but at higher doses (5 and 10 micrograms) it produced a significant rise in these levels. Phenoxybenzamine (0.05-10 micrograms, i.c.v.) caused a dose-related increase in corticosterone secretion. Pretreatment of rats with yohimbine considerably antagonized (up to 70%) the increase of corticosterone response induced by clonidine. Phenoxybenzamine failed to alter this effect. The depletion of brain catecholamines by alpha-methyl-p-tyrosine caused an increase in serum corticosterone concentration. The rise was suppressed by clonidine (10 micrograms, i.c.v.), and this suppression was antagonized in part by pretreatment with yohimbine. These data support the concept of the noradrenergic inhibition of ACTH secretion in rats. It seems likely that clonidine injected i.c.v. induces stimulation of corticosterone through the activation of presynaptic alpha 2-adrenoceptors and inhibition of noradrenaline release. The clonidine-induced inhibition of corticosterone after alpha-methyl-p-tyrosine seems to be mediated by alpha-adrenoceptors located postsynaptically.

Adrenocorticotropic Hormone↗
PubMed1983

Central histaminergic stimulation of pituitary--adrenocortical response in the rat.

In conscious rats histamine, the H1-receptor agonist 2-pyridylethylamine (PEA), and the H2-receptor agonists dimaprit and impromidine given intracerebroventriculary (i.c.v.) increased the hypophyseal-adrenocortical response, evaluated indirectly through the corticosterone concentration in the blood serum. On a molar basis histamine was the most potent drug whereas its agonists were less potent in inducing an increased corticosterone response. Impromidine however, was far more active than dimaprit and PEA. The effect of histamine was significantly yet not totally antagonized by either mepyramine, a H1-receptor antagonist, or cimetidine, a H2-receptor blocker. The combination of mepyramine and cimetidine caused a considerably stronger inhibition than that induced by either antagonist given separately. Mepyramine impaired the corticosterone response to PEA, and the responses to impromidine and dimaprit were significantly diminished by cimetidine. The results suggest that i.c.v. histamine increases the pituitary-adrenocortical activity via both H1- and H2-receptors, and there seems to be no significant prevalence of either of these receptors in mediating this action of histamine.

Animals↗
PubMed1983

The effect of clonidine injected centrally on serum-free fatty acids and glucose concentration in the rat.

Clonidine administered intracerebroventricularly (ICV) to conscious rats induced a significant dose-dependent increase in serum free fatty acid (FFA) and blood glucose levels. The rise in FFA and glucose concentrations after a dose of 10 micrograms averaged 80%-100% of the control levels. The alpha-adrenoceptor antagonists yohimbine, phentolamine, and phenoxybenzamine, administered alone ICV, did not substantially influence the control FFA and glucose levels. A hyperlipemic response to clonidine (10 micrograms) was abolished by an ICV pretreatment with yohimbine and was strongly antagonized by phentolamine but not by phenoxybenzamine. The clonidine-induced hyperglycemia was significantly diminished by phentolamine and only partly by yohimbine, whereas phenoxybenzamine was ineffective here. The histamine H2-receptor antagonist cimetidine, given ICV, failed to change these effects of clonidine. It seems likely that clonidine, given ICV, induces hyperlipemic and hyperglycemic effects through the stimulation of central alpha-adrenoceptors but not histamine H2-receptors. The lipolytic action of the drug depends more on the activation of alpha 2-adrenoceptors.

Animals↗
PubMed1983

Central H1- and H2-histaminergic stimulation of pituitary-adrenocortical response under stress in rats.

In rats subjected to a mild stress of immobilization histamine, H1-receptor agonist 2-pyridylethylamine (PEA), and H2-receptor agonists, 4-methylhistamine (4-MHA) and dimaprit, given intraventricularly 60 min prior to stress, intensified the stress-induced increase of hypophyseal-adrenocortical response, evaluated indirectly through corticosterone concentration in blood serum. The effects were dose dependent and on a molar basis histamine and PEA were the most potent and 4-MHA and dimaprit were less effective, in this respect. The effect of histamine was almost totally blocked by both H1-receptor antagonists, mepyramine or chloropyramine, and by H2-receptor antagonists, metiamide or cimetidine. The corticosterone response to PEA was abolished by mepyramine, and the responses to 4-MHA or dimaprit were antagonized by cimetidine and metiamide. The response to the H1 agonist was not substantially altered by pretreatment with cimetidine, and the responses to the H2 agonists were not changed by mepyramine. These results suggest that in stressed rats the corticosterone response to histamine is mediated by both H1 and H2 central histamine receptors.

Animals↗
PubMed1983

Effect of metiamide, a histamine H2-receptor antagonist on reserpine-induced gastric ulcers and acid secretion.

The effect of metiamide on reserpine-induced gastric ulcers and on gastric secretion during 6 h after ip administration was investigated in conscious intact rats and in rats with chronic gastric fistula. Reserpine, 3 mg/kg ip increased substantially the concentration of gastric acid in the first 4 h. Metiamide given every 3 h in a low dose (0.01 mumol/kg) intensified reserpine-induced gastric ulcers and also significantly increased the reserpine-induced acid concentration and output. In larger doses, (50-100 mumol/kg) metiamide considerably diminished gastric ulcer development and decreased gastric acid concentration. Given every 2 h metiamide in doses of 50-100 mumol/kg almost completely abolished gastric ulcer formation and markedly reduced the secretion of gastric acid in reserpinized rats. Anti-ulcer effect of metiamide was stronger than its antisecretory action, suggesting also the antiulcer action of metiamide other than inhibition of acid secretion. The results suggest that in conscious rats histamine H2-receptors are involved in reserpine-induced gastric ulcer development and gastric acid secretion. The antiulcer effect of metiamide may in part depend on its antisecretory action.

Animals↗
PubMed1981

Lipolytic responses induced by intracerebroventricular administration of histamine in the rat.

Histamine (10-50 microgram) administered intraventricularly in conscious rats induced an increase in serum-free fatty acids. The maximum, significant increase appeared 30-60 min after administration. Histamine H1-receptor antagonists, mepyramine and chloropyramine, when injected 2 h prior to histamine, abolished considerably hyperlipaemic responses to histamine. H2-Receptor antagonists, metiamide and cimetidine, given i.c.v. only moderately diminished histamine-induced hyperlipaemia. Histamine injected i.c.v. also increased serum corticosterone levels considerably. This elevation was prevented significantly by the H1-receptor antagonist, mepyramine, but not by the H2-receptor blocker, cimetidine. It seems likely that histamine given i.c.v. induces lipolysis through the release of ACTH, one of the known lipid-mobilizing hormones. The central lipid-mobilizing mechanism after histamine depends more on activation of H1- than H2-receptors.

Animals↗
PubMed1981

The involvement of central histamine receptors in stress-induced responses of serum corticosterone and free fatty acids and in gastric ulcer development.

Mild stress of restraint for 10 min at an ambient temperature of 18 degrees C increased serum corticosterone levels in rats considerably. Histamine given intravenously prior to restraint alone significantly further intensified the stress-induced elevation of serum corticosterone. Dimaprit and cimetidine failed to modify corticosterone responses to the mild stress. Severe stress of restraint and cold of 3 h duration increased serum corticosterone and free fatty acid levels considerably. Histamine given prior to stress exposure left the corticosterone and hyperlipaemic responses to severe stress unchanged. Dimaprit inhibited and cimetidine intensified the stress-induced hyperlipaemia. The most striking finding in the present experiment was a powerful inhibition of gastric stress ulcer generation by intraventricularly administered histamine. Dimaprit was similarly effective. This strong anti-ulcer effect of histamine was abolished by intraventricular pretreatment of rats with either H1- or H2-receptor antagonists, chloropyramine or cimetidine. The results may suggest that in the rat a mild stress does not fully activate central histaminergic pathways involved in corticosterone responses. During severe stress histamine considerably prevents gastric ulcer generation and both H1- and H2-receptors mediate this action of histamine.

Animals↗
PubMed1981

The role of central histamine H1- and H2-receptors in hypothermia induced by histamine in the rat.

Histamine administered intraventricularly or into the anterior hypothalamic preoptic region induced dose-dependent hypothermia in rats with chronic i.c.v. cannula. This hypothermia was almost totally abolished by both the histamine H1- and H2-receptor antagonists, mepyramine or chloropyramine and metiamide or cimetidine, respectively, give i.c.v. prior to histamine. In behavioural thermoregulation studies histamine considerably diminished the mean duration of dwelling of the rat under the heat lamp. This effect was abolished by histamine H1- but not by H2-receptor antagonists. It is concluded that histamine induces hypothermia by lowering the set point of the hypothalamic thermostat by means of H1-receptors. Histamine H2-receptor blockers antagonized the increase in tail skin temperature after histamine administration, suggesting that h2-receptors are involved in a heat loss mechanism.

Animals↗
PubMed1979

Physiological and morphological characteristics of progressive disruption of the canine gastric mucosal barrier.

The investigation had two major goals: to define the progression of physiological changes associated with disruption of the gastric mucosal barrier to sodium and hydrogen and to identify the morphological correlates of the physiological alterations. Fluxes of ions and water were determined before and after treatment of oxyntic mucosa with graded concentrations of butyric acid using dogs with gastric pouches. Three phases of barrier disruption were characterized: I, acceleration of normal Na+/H+ exchange; II, neutralization of H+; III, exudation of interstitial fluid. Parallel studies assessed morphological damage associated with these phases. In Phase I, cellular bulging into the lumen and dilation of intercellular spaces were evident. Some cellular erosion and extreme intercellular dilation were prominent in Phase II. Phase III was represented by necrotic changes and desquamation. It is concluded that disruption of transport mechanisms occurs sequentially and is closely correlated with morphological signs of progressive damage.

Animals↗
PubMed1977

The action of serotonin on basal gastric secretion in the conscious rat after intraventricular and intraperitoneal administration.

In unanesthetized rats with chronic gastric fistulas the effect of various doses of 5-HT and atropine given intraperitoneally (i.p.) or into the lateral cerebral ventricle (i.c.) on basal gastric secretion was investigated. 5-HT given i.e. reduced HCl secretion more strongly than by the i.p. route. Atropine reduced gastric secretion equally after i.p. or i.e. administration. 5-HT given i.p. or i.c. produced a weaker inhibitory effect on basal gastric acid secretion than atropine. The stronger antisecretory action of 5-HT after i.c. than after i.p. administration indicates that the amine directly depresses the vegetative brain centers responsible for the basal secretory activity of the gastric mucosa.

Animals↗
PubMed1976

Effect of metiamide, a histamine H2 - receptor antagonist, on the development of gastric stress ulcers and acid secretion.

In normal and stressed rats with chronic gastric fistula small doses of metiamide (0.001-0.01 muM/kg) increased and doses of over 20 muM/kg decreased gastric acid secretion. In both these dose ranges of dosage metiamide suppressed the development of stress ulcers, most markedly in doses of 0.005 and 100 muM/kg. Intermediate doses had no such action. Only the anti-ulcer action of large doses of metiamide ran parallel to a reduction in acid secretion. Small doses of metiamide increased gastric secretion, but like larger doses, had a weak adrenergic action.

Animals↗