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Biomedical subjects

B Cuparencu

Publications and source records attributed to B Cuparencu.

At least 19 recordsLinked to original sources
PubMed2001

Effects of zopiclone on blood glucose level, serum lipid concentration and clot lysis time in normoglycemic and normolipidemic rats.

In normoglycemic and normolipidemic rats the i.p. injection of zopiclone induced an acceleration of fibrinolysis in a dose-dependent bell shaped manner and various changes of the blood glucose level. Total lipids, total cholesterol and triglyceride serum levels remained unaffected by doses of 1.25, 2.5 and 15.0 mg/kg, with the exception of the medium dose (5.0 mg/kg) and the next dose (10.0 mg/kg) which lowered them very significantly.

Animals↗
PubMed2000

The influence of intracerebroventricular administration of (+/-) propranolol and (+/-) verapamil on experimental myocardial ischemia and necrosis in rats.

In albino rats, infarctoid myocardial lesions were produced by intraperitoneal (i.p.) administration of isoproterenol (75 mg/kg, during 3 days). In other groups, the descending anterior left coronary artery was ligated. In both experimental settings, the intracerebroventricular (i.c.v.) administration of (+/-) propranolol (100-200-300 microg/animal/day, during 7 days) or (+/-) verapamil (40-80-160 microg/animal/day, during 7 days) afforded a significant protection (with the exception of the lowest dose) on the investigated parameters: arrhythmias, ischemic zone (in coronary ligated rats), lactate dehydrogenase and aspartate aminotransferase activity of the serum, focal necrosis (in isoproterenol treated rats). This protective activity is lower than that afforded by i.p. administered (+/-) propranolol (5 mg/kg, during seven days) or (+/-) verapamil (5 mg/kg, during seven days). From these data it may be concluded that (+/-) propranolol and (+/-) verapamil have a protective action on the experimental myocardial ischemia and necrosis in rats, not only when the drugs come in direct contact with the heart, but also acting upon the central nervous system.

Animals↗
PubMed2000

Effects of ICI 118.551, a selective beta-2 adrenergic blocking agent on the guinea pig cardiac excitability and ventricular fibrillation threshold.

In isolated guinea pig perfused hearts ICI 118.551, a selective beta 2 adrenoceptor antagonist, induced transient ventricular extrasystoles. Following the termination of the perfusion, a very significant increase of both the ventricular fibrillation threshold and the refractory periods were measured. In guanethidine pretreated hearts, ICI 118.551 failed to induce premature beats. At the same time the fibrillation threshold and refractory periods exhibited a very significant decrease. The perfusion of equimolecular concentration of metoprolol, a beta-1-adrenoceptor antagonist, and (+) propranolol, a quinidine-like compound, induced, in most experimental settings, similar results as ICI 118.551. Thus, besides its beta-2-adrenoceptor antagonist properties, ICI 118.551 presented other pharmacological actions.

Adrenergic beta-Antagonists↗
PubMed2000

Acute effects of zopiclone on blood glucose level and serum lipids in hyperlipidemic rats. Interactions with PK 11195 and flumazenil.

UNLABELLED: Intraperitoneal administration of 5 mg/kg zopiclone a cyclopyrolone acting on the central benzodiazepine receptors was found to produce significant reduction of total lipids, total cholesterol and triglyceride in rats randered hyperlipidemic by intraperitoneal injection of Triton W-1339. Blood glucose level was also reduced. Flumazenil (10 mg/kg) potentiated the hypoglicemic effect of zopiclone but had no additional effect on serum lipids. PK 11195 (25 mg/kg) antagonized the hypolipidemic effects of zopiclone. IN CONCLUSION: 1. The central benzodiazepine receptors are not involved in the hypolipidemic activity of zopiclone. 2. The peripheral type benzodiazepine receptors are partly responsible, for the hypolipidemic activity of this cyclopirrolone. 3. The changes of blood glucose level induced by these drugs does not seem to be related to benzodiazepine receptors.

Animals↗
PubMed2000

Acute effects of zopiclone on blood glucose level and serum lipids in hyperlipidemic rats.

In rats rendered hyperlipidemic by ip administration of Triton WR-1339, the ip administration of zopiclone at doses of 1.25, 2.5, 5.0, 7.5, 10.0 and 15.0 mg/kg, a cyclopyrrolone acting upon the central benzodiazepine receptors, induces very significant reductions of total lipids, total cholesterol, and triglycerides, at nearly all of the doses. The most active dose was 5.0 mg/kg. The blood glucose level was diminished by doses of 1.25, 2.5, 7.5 and 15.0 mg/kg and it was not changed by the rest of the other doses.

Animals↗
PubMed1996

Effects of midazolam on glycemia and serum lipids in rats.

Midazolam administered ip. in albino rats (each group consisted from 10 animals rendered hyperdyslipidemic by the administration of Triton WR-1339) induced at most doses a significant reduction of glycemia (p < 0.001). However, the reduction of blood glucose level was outside of the dangerous level. Midazolam elicited also very significant decrease of the elevated serum lipids (p < 0.001). The pharmacological analysis of these phenomena by using the peripheral type benzodiazepine (BZD) receptors antagonist PK 11105, the central BZD receptor antagonist flumazenil and the purinergic P1 receptors antagonist aminophylline has shown that the effects on serum lipids were due, very probably to the stimulation of the peripheral type BZD receptors. Aminophylline seems to have the property to block the peripheral type BZD receptors. The effects on blood glucose level were very variable.

Aminophylline↗
PubMed1995

Effects of 4'-chlordiazepam on glycemia and serum lipids in hyperlipidemic rats: interactions with PK 11195 and flumazenil.

In rats rendered hyperlipidemic by the interperitoneal injection of Triton WR-1339, the administration of 4'-chlorodiazepam, a selective agonist of the peripheral type of benzodiazepine (BZO) receptors evoked significant reductions of serum lipids. PK 11195, a specific antagonist of these receptors, partially inhibited these effects. Flumazenil, a selective antagonist of the central BZD receptors, enhanced the lipid lowering activity of 4'-chlorodiazepam.

Animals↗
PubMed1994

Effects of the intracerebroventricular administration of ketamine on centrogenic arrhythmias in anesthetized rats.

In urethane anesthetized rats the icv (lateral cerebral ventricle) administration of ketamine, at the highest utilized doses, induced bradypnea and sinus bradycardia in spontaneously breathing rats. Moreover, it partially antagonized the arrhythmogenic activities of sodium glutamate and sodium aspartate, as well as desipramine and ouabain. From these results, we conclude that ketamine had an inhibitory effect on the centrogenic arrhythmias not only acting at the level of NMDA subtype receptor, but also at beta 1 adrenergic central receptors. Moreover at high doses, ketamine can also induce centrogenic arrhythmias in spontaneously breathing rats.

Anesthesia↗
PubMed1992

Effects of gadolinium on N-methyl-D-aspartate (NMDA)-induced centrogenic arrhythmias.

In urethane-anesthetized rats, the intracerebroventricular (i.c.v.) administration of N-methyl-D-aspartate (NMDA)-induced central arrhythmias. These cardiac rhythm disorders could be prevented by the i.c.v. microinjection of gadolinium, an inhibitor of exocytosis. These findings suggest that inhibition of central neurotransmitter exocytosis could protect against centrogenic arrhythmias.

Anesthesia↗
PubMed1992

Inhibitory role of somatostatin on calcitonin secretion.

Calcitonin (CT) secretion is not exclusively controlled by calcemia, but the secretory tonus is maintained by the beta-stimulatory adrenergic system Somatostatin (SMS) plays a neuromodulatory role with the reduction of CT secretion by its interference at the central and peripheral level of the beta adrenergic receptors. The experiments were carried out on groups of rats in which the effect of SMS on CT content of the thyroid gland was followed up. Thus, SMS administered i.c.v. significantly reduced the basal CT secretion without blocking the stimulatory effect of calcium. The results were comparable with those obtained after the blockade of the sympatho-adrenergic system by chemical sympathectomy with 6HODA or propranolol. Central blockade of alpha receptors with phentolamine determined a significant rise of CT. This effect was annihilated by SMS. The i.v. administration of SMS did not induce a change in CT content of the thyroid, but blocked the stimulatory action of hypercalcemia. The results are identical with those obtained by blocking the beta-receptors with propranolol. SMS also blocked the stimulatory effects of isoproterenol on CT secretion. The data obtained revealed the fact that SMS lowers CT secretion by the central and peripheral interference of the sympatho-adrenergic path, maintaining the secretory tonus of the thyroid C cells.

Animals↗
PubMed1992

Central arrhythmogenic effects of N-methyl-D-aspartate (NMDA) in anesthetized rats: influence of the denervation of the carotid-sinus baroreceptors on the susceptibility to arrhythmias.

The intracerebroventricular (i.c.v.) administration of NMDA into urethane anesthetized rats could induce centrogenic cardiac arrhythmias. There were some important differences between sodium glutamate- and NMDA-induced arrhythmias which rendered it difficult to accept the assumption that glutamate-induced arrhythmias were due to the stimulation of only NMDA receptors. Denervation of the carotid-sinus baroreceptor zones enhanced the central arrhythmogenic activity of both sodium glutamate and NMDA.

Anesthesia↗
PubMed1986

Central antiarrhythmic effects of imidazole in anesthetized rats.

In urethane anesthetized rats, the intracerebroventricular (icv.) microinjection of sodium glutamate or KCl induced cardiac arrhythmias. These cardiac rhythm disorders could be prevented by the icv. administration of imidazole. The i.v. injection of the same doses of imidazole elicited cardiac arrhythmias. The antiarrhythmic activity of imidazole is probably due to its ability to stimulate phosphodiesterase activity, which leads to a decrease in cGMP and/or cAMP cerebral levels.

Anesthesia↗
PubMed1986

Central antiarrhythmic activity of adenosine in anesthetized rats.

In urethane-anesthetized rats the intracerebroventricular (icv.) administration of sodium glutamate or desipramine induced cardiac arrhythmias. These cardiac rhythm disturbances could be prevented by icv. administration of adenosine. The i.v. injection of adenosine had an arrhythmogenic action. The antiarrhythmic effect of adenosine could be reversed by icv. aminophylline. It is suggested that the antiarrhythmic activity of adenosine is due to the central inhibition of release of acetylcholine, and/or noradrenalin, produced by the decreased availability of calcium for the excitation-secretion coupling.

Adenosine↗
PubMed1985

Experimental anti-ulcer activity of Veronica officinalis L. extracts.

In indomethacin-induced ulcers in albino rats, the anti-ulcerogenic effects of some extracts prepared from Veronica officinalis L. were investigated. The extracts had a significant anti-ulcerogenic activity. In ulcer healing experiments performed in rats by administering reserpine, the extracts were found to enhance the regeneration of the gastric mucosa. These results seem to confirm the popular observations according to which the decoction from Veronica officinalis L. possessed useful properties in the treatment of gastric ulcers.

Animals↗