Search PubMed⌕ Search

Biomedical subjects

J Bugajski

Publications and source records attributed to J Bugajski.

92 records · Page 6Linked to original sources

The effect of drugs interfering with biogenic amines metabolism on gastric secretion and reserpine-ulcers development in rats.

The effect of drugs interfering with endogenous catecholamines metabolism on gastric secretion and gastric ulcers development 4 hr following reserpine administration was investigated in rats with chronic gastric fistulas. Drugs inhibiting catecholamine synthesis: alpha-methyl-p-tyrosine (alpha-MT) and sodium diethyldithiocarbamate (DDC) decreased substantially the reserpine-induced gastric acid and pepsin secretion, but only alpha-MT diminished the development of gastric ulcers. Pretreatment with nialamide (NLD) elicited in reserpinized rats a marked inhibition both of gastric secretion and of gastric ulcers development. Dopamine (DA), noradrenaline (NA) and adrenaline (A) decreased the secretion of hydrochloric acid but did not change the intensity of gastric ulcers caused by reserpine. Desipramine strongly inhibited reserpine-induced gastric acid secretion. Reserpine depleted DA, NA and 5-HT stores in the brain and decreased DA and 5-HT levels in the wall of the stomach in which the NA levels were increased. The changes in biogenic amines content induced by drugs in reserpinized rats did not correlate with their influence on gastric secretion and on the development of mucosal ulcers. The inhibitory effect of all of the drugs examined on gastric acid and pepsin secretion in reserpinized rats was accompanied by the inhibition of gastric ulcers formation following NLD and alpha-MT administration only, indicating that ulcer generation following reserpine depends more on changes in mucosal barrier resistance than on gastric acid secretion.

Animals↗

Effect of catecholamines and adrenergic antagonists on blood glucose, free fatty acids and liver glycogen levels in fed rats.

In fed rats the effects of catechloamines and adrenergic antagonists on blood glucose, free fatty acids (FFA), and liver glycogen levels were investigated in order to determine the role of alpha- and beta-adrenergic receptors in metabolic responses to catechloamines. Hyperglycemic responses to dopamine (DA), noradrenaline (NA), adrenaline (A) and isoprenaline (ISP) were dose-related and accompained by a depletion of liver glycogen. The relative potencies in producing hyperglycemia and in causing liver glycogenolysis were in descending order of potency, A, NA, DA and ISP. Hyperlipemic response was most potent to NA and DA, weaker to ISP, and least potent to A. Phentolamine antagonized completely both hyperglycemia and hepatic glycogen depletion induced by all catecholamines. Propranolol impaired only hyperglycemic responses to A and ISP. Phentolamine antagonized hyperlipemia induced by DA and NA but only partially impaired hyperlipemia after A. Propranolol only partially antagonized hyperlipemic responses to NA and ISP without influencing DA--and A-induced hyperlipemia. The results indicate that in fed rats hyperglycemic responses to catecholamines are mediated mainly by an alpha-adrenergic receptor, and hyperlipemic responses do not fit inton the alpha-receptor or beta-receptor classification.

Animals↗