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Biomedical subjects

T Torda

Publications and source records attributed to T Torda.

At least 19 recordsLinked to original sources
PubMed1995

Alcohol, corticosteroids, energy utilization, and hippocampal endangerment.

The cellular weakening or cytoxic consequences of CAC are intertwined in the most fundamental sense with energy intake, production, storage, and mobilization. The impact of CAC on the HPA axis to increase GCs makes this energy regulatory hormone along with pancreatic hormones a potential major player in the site-specific organ pathologies associated with CAC. Although little is known about the mechanism of CAC neurotoxicity, the hippocampal endangerment model which relies heavily on the cellular weakening, site-specific effect of continuous or chronic, intermittent (withdrawal, binge drinking) elevation of GCs, even less is known about the mechanism of neurotoxicity of activating the ethanol-inducible CYP2E1 system. It is likely that components of both models contribute to the site-specific, CNS neurotoxicity associated with CAC, but this remains largely unresolved.

Adrenal Cortex Hormones↗
PubMed1994

In-vitro interaction between H2 antagonists and vecuronium.

The interaction between histamine H2 antagonists and the neuromuscular blocking drug vecuronium was investigated in the rat phrenic nerve-hemidiaphragm preparation. Cimetidine alone, in the concentration range 800-4000 microM produced between 14 and 74% neuromuscular paralysis with an EC50 (mean +/- s.e.) of 2900 +/- 100 microM. Ranitidine augmented the indirectly-evoked muscle response at concentrations between 30 and 160 microM but at higher concentrations, between 300 and 1800 microM, produced neuromuscular paralysis. Famotidine produced negligible and statistically insignificant (0-5%) neuromuscular paralysis at concentrations between 0.3 and 300 microM. Cimetidine (800 microM) shifted the neuromuscular concentration-effect curve of vecuronium to the left in a parallel manner, while ranitidine (160 microM) shifted it to the right. The potentiation ratio was 1.90 +/- 0.14 for cimetidine and 0.62 +/- 0.05 for ranitidine. Famotidine (30 microM) did not alter the response to vecuronium. These data indicate that higher than clinically relevant concentrations of cimetidine and ranitidine produce neuromuscular paralysis and may potentiate the action of vecuronium. Low concentrations of ranitidine may antagonize the action of vecuronium. Famotidine, in contrast, lacks significant neuromuscular effects.

Animals↗
PubMed1993

Cross-linking of iodinated prolactin to rat liver nuclear protein.

The specific binding of prolactin (PRL) in rat liver nuclei have been examined. Following cross-linking with the use of 125I-rat prolactin and autoradiography the evidence is presented for the specific binding of PRL to a nuclear protein with low Mr of about 7000. This study shows that the PRL binder in rat liver nuclei is a small protein and probably differs from molecular form of the rat liver membrane prolactin receptor.

Animals↗
PubMed1992

Propofol and ECT.

Explore the source record for details and available documents.

Electroconvulsive Therapy↗
PubMed1991

Increased beta 2-adrenoceptors in the superior cervical ganglia of genetically hypertensive rats.

[125I]Iodocyanopindolol binding sites were characterized by autoradiography in the superior cervical ganglia of Wistar-Kyoto (WKY) rats. A high concentration of (-)-[125I]iodocyanopindolol binding sites, characterized as beta-adrenoceptors by (-)-propranolol displacement, was distributed throughout the ganglia and in the postganglionic (internal carotid) nerve. ICI 118,551, a beta 2-selective antagonist, displaced more than 85% of the binding sites, whereas CGP 20712A, a beta 1-selective antagonist, displaced less than 10% of the binding sites, indicating that the beta-adrenoceptors were primarily of the beta 2-subtype. Emulsion autoradiography demonstrated that at least part of the binding sites were associated with principal ganglion cells. Unilateral deafferentation did not modify the number of binding sites in the superior cervical ganglia of WKY or spontaneously hypertensive rat (SHR). These results suggest that at least part of these receptors may correspond to prejunctional beta 2-adrenoceptors originated in principal ganglion cells. The concentration of beta 2-receptors was increased in the superior cervical ganglia of young and adult SHR when compared to age-matched WKY rats (49% and 39%, respectively). There were no differences in beta 2-adrenoceptor number in the stellate ganglia of young and adult WKY and SHR. These results suggest that beta 2-adrenoceptor stimulation may be selectively enhanced in some peripheral sympathetic ganglia in SHR and this could play a role in the development and maintenance of the increased sympathetic activity in this strain.

Adrenergic beta-Antagonists↗
PubMed1991

A graded combination regimen for maintenance of gastric pH above 3.5 in critically ill patients.

Prophylaxis of acute upper gastrointestinal bleeding by control of gastric pH has been widely advocated for intensive care patients. H2-blockers and antacids have been used and demonstrated to be incompletely effective at maintaining gastric pH above 4. A study of 100 patients measured the efficacy of two-hourly gastric pH measurement and titrated therapy consisting of five levels: 1. no therapy 2. ranitidine 50 mg 8 hourly intravenously 3. ranitidine plus Mylanta 30 ml 2 hourly by nasogastric tube 4. ranitidine plus Mylanta 60 ml 2 hourly and 5. ranitidine 100 mg 8 hourly intravenously plus Mylanta II 60 ml 2 hourly. The level of treatment required by proportions of the total study group were (1) 15%, (2) 71%, (3) 96%, (4) 100%. Head-injured and intubated patients generally fell in the more resistant group while patients having had major elective surgery required lower levels of therapy. If control of gastric pH is to be uniformly achieved, a technique of titrated therapy based on gastric pH measurements is supported as cheaper and more effective than other standardised treatment regimens.

Adult↗
PubMed1991

Propofol as an anaesthetic agent for ECT: effect on outcome and length of course.

Recent reports of reduced seizure duration with ECT under propofol anaesthesia have led to concerns that propofol may diminish the efficacy of this treatment. To investigate the effect of propofol on the response to ECT, we reviewed records of 66 patients with primary depression treated with ECT, 37 of whom had been assessed prospectively with pre- and post-ECT Hamilton and Zung depression severity ratings. Despite demonstrating that the individual seizure duration was significantly reduced with propofol compared to thiopentone we found no evidence of reduced ECT efficacy with propofol. Courses under propofol anaesthesia were on an average two treatments longer than with thiopentone. Although this difference was not statistically significant this may have been due to a type II error. These results suggest that it is premature to abandon the use of this new anaesthetic agent in ECT without controlled prospective outcome studies.

Adult↗
PubMed1990

Adrenergic regulation of [3H]ketanserin binding sites during immobilization stress in the rat frontal cortex.

Acute immobilization stress increased serotonin and 5-hydroxyindoleacetic acid levels, the 5-hydroxyindoleacetic/serotonin ratio, and the number of [3H]ketanserin binding sites, representing serotonin-2 type receptors, in the rat frontal cortex. Peripheral administration of propranolol or central administration of 6-hydroxydopamine abolished the stress induced elevation of [3H]ketanserin binding sites. Treatment with 6-hydroxydopamine did not affect the increase in serotonin and 5-hydroxyindoleacetic acid levels, and enhanced the increase in the 5-hydroxyindoleacetic acid/serotonin ratio produced by stress. Conversely, chemical serotoninergic denervation with 5,7-dihydroxytryptamine had no influence on the stress-induced elevation of [3H]ketanserin binding sites, but abolished the serotonin and 5-hydroxyindoleacetic acid increase produced by stress. These results suggest that an intact serotoninergic system is not essential for serotonin-2 type receptor regulation during stress. Instead, the noradrenergic system, most probably through stimulation of beta-adrenoreceptors, may control the regulation of [3H]ketanserin binding sites in the rat frontal cortex during acute stress.

Animals↗
PubMed1990

Effect of the anesthetic agent propofol on hormonal responses to ECT.

Propofol is a new anesthetic induction agent that reduces electroconvulsive therapy (ECT) seizure duration. To indirectly investigate the effect of propofol on ECT-induced acute central neurotransmitter changes, we studied neuroendocrine responses in 25 primary depressed subjects treated with ECT under either propofol or thiopentone anesthesia. Blood samples were taken prior to ECT, and then at regular intervals for 2 hr. Only the prolactin response correlated significantly with seizure duration (r = 0.52, p less than 0.01). Subjects given propofol had significantly reduced adrenocorticotropin (ACTH) (p less than 0.01) and cortisol (p less than 0.05) responses compared to thiopentone, which were independent of seizure duration. There was a trend towards a reduction in the prolactin response with propofol compared to thiopentone, but this was dependent upon the diminished seizure duration. The results indicate that propofol affects endocrine responses to ECT by two distinct mechanisms: decreasing prolactin by reducing the seizure duration and decreasing ACTH and cortisol by another process, possibly via a reduction in central noradrenergic activation.

Adrenocorticotropic Hormone↗
PubMed1990

Increased beta 2-adrenoceptor number in peripheral sympathetic ganglia of spontaneously hypertensive rats.

We determined beta-adrenoceptor concentrations in sympathetic ganglia from adult Spontaneously Hypertensive Rats (SHR) and Wistar-Kyoto (WKY) control rats by quantitative autoradiography. Adjacent tissue sections were incubated with [125I]iodocyanopindolol, with or without excess of unlabeled (-)-propranolol, the beta 1-antagonist CGP 20712A or the beta 2-antagonist ICI 118,551. Most beta-adrenoceptors were of the beta 2-type. Their concentration was higher in the superior cervical and stellate ganglia of SHR when compared to normotensive WKY. Our results indicate that beta 2-adrenoceptor stimulation may be enhanced in sympathetic ganglia of SHR, and could play a role in the maintenance of their increased sympathetic activity.

Animals↗
PubMed1990

Enhanced phosphoinositide hydrolysis in the pineal gland of spontaneously hypertensive rats.

We studied the phosphoinositide (PI) turnover in the pineal gland of spontaneously hypertensive rats (SHR) and compared it to that in Wistar-Kyoto and Wistar rats. Both basal and norepinephrine-stimulated PI turnover were significantly higher in the SHR than in the other strains. Prazosin (1 mumol/L) completely blocked the norepinephrine-induced PI hydrolysis in all groups. However, prazosin failed to lower the enhanced basal PI turnover in SHR. Pineal response to the cholinergic agonist carbachol was similar in all groups. These results suggest enhanced membrane phospholipid turnover in the pineal gland of SHR. Moreover, signaling via the alpha 1-adrenoceptor might be sensitized in the SHR.

Animals↗
PubMed1990

Determination of guanine nucleotide sensitivity of [125-I]-neuropeptide Y binding in the rat pituitary gland by quantitative autoradiography.

[125I]-neuropeptide Y receptors were characterized in the rat pituitary gland using quantitative autoradiography. Scatchard analysis of saturation isotherms showed high affinity (Kd 8.5 x 10(-11) M) and single class of binding sites (Bmax 0.22 pmol/mg of protein) in the posterior lobe of the pituitary gland, with no specific binding in the intermediate or anterior lobe. Increasing concentrations of guanine nucleotide analogues and peptide YY inhibited neuropeptide Y binding. In addition, neuropeptide Y binding was pertussis-toxin-sensitive. These results add additional information about a possible neuronal (through neuropeptide Y) and hormonal (through peptide YY) regulation of posterior pituitary function, which is most probably GTP-dependent.

Animals↗
PubMed1989

Pineal muscarinic phosphoinositide response: pertussis toxin resistant signaling with very low receptor number.

Autoradiography revealed very low density of muscarinic receptors in the rat pineal gland. Yet, the magnitude of phosphoinositide hydrolysis elicited with 0.1 mM carbachol was similar to that seen with 1 mM norepinephrine. The cholinergic and adrenergic phosphoinositide responses were fully additive. The cholinergic signal was insensitive to pertussis toxin both in vivo and in vitro and persisted in pineals cultured for 5 days. The data expand our previous finding on functional muscarinic acetylcholine receptors in the rat pineal gland.

Animals↗
PubMed1989

Brain natriuretic peptide receptors in the rat peripheral sympathetic ganglia.

High affinity binding sites for brain natriuretic peptide were characterized in the rat superior cervical ganglia by quantitative autoradiography. In addition, the peptide increased the formation of cyclic GMP in the ganglia in vitro. Brain natriuretic peptide displaced atrial natriuretic peptide from its binding sites. Our results suggest that brain natriuretic peptide and atrial natriuretic peptide may share physiologically active receptors in sympathetic ganglia. Brain natriuretic peptide may modulate the synaptic transmission in sympathetic ganglia, in addition or in conjunction with atrial natriuretic peptide.

Animals↗
PubMed1989

Cholinergic stimulation of phosphoinositide hydrolysis in the rat pineal gland.

Carbachol induced a dose-dependent accumulation of inositol monophosphates in the Wistar rat pineal gland. The relative potency of muscarinic antagonists (atropine greater than pirenzepine much greater than gallamine) in blocking this response suggests the involvement of muscarinic M1 receptors. Following bilateral superior cervical ganglionectomy, the carbachol-induced phosphoinositide response was similar to that seen in sham-operated controls, while adrenergic response was enhanced by 50%. The results indicate that the pineal has functional muscarinic receptors which are not affected by removal of the sympathetic innervation to the gland.

Animals↗
PubMed1989

Characterization of beta 1- and beta 2-adrenoceptor subtypes in the rat sinoatrial node and stellate ganglia by quantitative autoradiography.

We characterized beta-adrenoceptors in rat sinoatrial node (SA) and stellate ganglia by incubating consecutive tissue sections with [125I]iodocyanopindolol, with or without the beta 1-selective (CGP 20712A) or the beta 2-selective (ICI 118,551) antagonists, followed by quantitative autoradiography. In the stellate ganglia, ICI 118,551 displaced more than 90%, and CGP 20712A less than 5%, of the binding sites. CGP 20712A displaced about 50% of the binding sites in the SA, and about 65% in the rat atria. The SA has a high percentage of beta 2-adrenoceptors and the stellate ganglia contains almost exclusively beta 2-adrenoceptor binding sites, implicating beta 2-adrenoceptors in the control of heart rate in the rat.

Animals↗
PubMed1989

Autoradiographic characterization of beta-adrenoceptors in rat heart valve leaflets.

beta-Adrenoceptors were localized and characterized in valve leaflets of the rat heart. Sixteen micrometer-thick tissue sections containing the mitral and aortic valves were incubated with (-)3-[125I]iodocyanopindolol followed by autoradiography with computerized microdensitometry and comparison with 125I-labeled standards. beta-Adrenoceptors were present in all the valves studied. The selective beta 1-adrenoceptor antagonist CGP 20712 A (100 nM) displaced not more than 20% of the total binding sites, suggesting that most of the beta-adrenoceptors in the valve leaflets are of the beta 2-subtype. Forskolin-binding sites were detected in the mitral valve leaflet by incubation of adjacent tissue sections with [12-3H]forskolin. Our results indicate that catecholamines could regulate the function of the heart valves through stimulation of beta 2-adrenoceptors.

Animals↗