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Biomedical subjects

E Costa

Publications and source records attributed to E Costa.

At least 721 records · Page 40Linked to original sources
PubMedDate not supplied

Levonantradol-induced inhibition of acetylcholine turnover in rat hippocampus and striatum.

The effects of levonantradol, a structural novel cannabinoid-related analgesic, on the turnover rate of acetylcholine (TRACh) have been studied in various regions of the rat brain. Levonantradol (0.3 mg/kg subcutaneously) decreases the tRACh in the hippocampus and striatum by 53 and 30 per cent, respectively. The extent of the reduction in TRACh is dose dependent, with a maximal decrease of 80 per cent in the hippocampus and 57 per cent in the striatum following the 3 mg/kg dose. In contrast, cortical TRACh is not affected by any dose of levonantradol. This pattern of activity on cholinergic dynamics elicited by levonantradol is qualitatively similar to that of cannabinoids but differs from that previously reported for narcotic analgesics. Moreover naltrexone (2 mg/kg intraperitoneally) does not reverse the effects of levonantradol on striatal or hippocampal TRACh. This pattern of activity on cholinergic dynamics elicited by levonantradol is consistent with a cannabinoid-like rather than an opioid-like mode of action.

Acetylcholine↗
PubMedDate not supplied

Comparison of different regimens of glucocorticoid replacement therapy in patients with hypoadrenalism.

Since the optimal glucocorticoid replacement needs to avoid over and under treatment, the adequacy of different daily cortisone acetate (CA) doses was assessed in 34 patients with primary and central hypoadrenalism. The conventional twice CA 37.5 mg/day dose was administered to all patients (A regimen: 25 mg at 07:00 h, 12.5 mg at 15:00 h), while in 2 subgroups of 12 patients the dose was shifted on 2 thrice daily regimens (B: 25 mg at 07:00, 6.25 mg at 12: 00, 6.25 mg at 17:00; C: 12.5 mg, 12.5 mg, 12.5 mg). In other 12 patients the conventional dose was reduced to a thrice 25 mg/day administration (D regimen: 12.5 mg, 6.25 mg, 6.25 mg). In all patients, urinary free cortisol (UFC) excretion and cortisol day curves were evaluated. During the CA 37.5 mg administration, nadir cortisol levels were significantly higher with the thrice daily regimens (143 +/- 31 on B and 151 +/- 34 nmol/l on C) than with the conventional twice (85 +/- 16 nmol/l). Moreover, UFC, morning cortisol levels and mean cortisol day curves were similar in each group. Finally, during D regimen nadir cortisol levels were higher than in A and similar to B and C regimens. No difference in UFC and in cortisol day curves by reducing the CA dose was found. In conclusion, the thrice daily cortisone regimens, in which more physiological cortisol levels are achieved, perform better as replacement therapy. The administration of 25 mg/day CA confirms that replacement therapy is more adequate with a lower dose, particularly in patients with central hypoadrenalism.

Adrenal Insufficiency↗
PubMedDate not supplied

Distribution of met5-enkephalin-Arg6-Phe7 (MEAP) in various tissues of rats and guinea pigs.

With a specific and sensitive radioimmunoassay coupled to HPLC separation, we have measured met5-enkephalin-Arg6-Phe7 in extracts of various peripheral organs. The highest content was found in ileum and lung. The MEAP in lung can be released in a Ca++-dependent manner by KCl. The ratio of MEAP/ME seems to differ in various peripheral tissues, suggesting that MEAP may not only be a precursor of ME but may also act as a neurotransmitter or neuromodulator itself.

Animals↗
PubMedDate not supplied

Study of the release mechanism of diltiazem hydrochloride from matrices based on chitosan-alginate and chitosan-carrageenan mixtures.

The aim of this work was to establish the diltiazem hydrochloride release mechanism from the chitosan-alginate matrix tablet (MCB/AS) and chitosan-carrageenan matrix tablet (MCS/CSI). The weight loss for MCS/CSI is mainly due to the weight loss of the matrix while for MCB/AS it is mainly due to the diltiazem hydrochloride released from the tablet. Using the Peppa's model the release order for MCS/CSI was n = 1.07 +/- 0.13 and for MCB/AS was n = 0.76 +/- 0.02. Thus, MCS/CSI has a transport mechanism, and for MCB/AS the drug release mechanism is a combined process of diffusion and relaxation. MCB/AS has an elastic modulus (G' = 10(5) Pa) one order of magnitude higher than MCS/CSI (G' = 10(4) Pa). MCB/AS is able to uptake solvent without disrupting the microstructure due to its high elastic modulus. Instead MCS/CSI showed a quick erosion process, which conducted to the tablet disintegration due to a fast solvent uptake process.

Alginates↗
PubMedDate not supplied

The regulation of hippocampal nicotinic acetylcholine receptors (nAChRs) after a protracted treatment with selective or nonselective nAChR agonists.

In rats, 1 mg/kg twice daily for 10 d of nicotine, a nonselective agonist of nicotinic acetylcholine receptors (nAChRs), fails to change alpha4 and beta2 nAChR subunit mRNA but significantly decreased alpha7 nAChR subunit mRNA and protein expression, which is associated with a 35-40% decrease in the number of 125I-alpha-Bgtx binding sites in hippocampus. In addition, this schedule of nicotine treatment produced a 40% increase in the number of high- (K(D) 1 nM), but decreased by 25% the number of low-affinity (K(D) 30 nM) binding sites for 3H-epibatidine in hippocampus. In contrast, repeated treatment with lobeline (2.7 mg/kg twice daily for 10 d), which selectively binds to high-affinity binding nAChRs, fails to change the expression of high- or low-affinity nAChRs. These data suggest that a simultaneous upregulation of high-affinity nAChRs and downregulation of low-affinity nAChRs is elicited by ligands that can bind to both low- and high-affinity nAChRs, but not by selective agonists of high-affinity nAChRs. One might infer that in hippocampus, high- and low-affinity nAChRs may be located in the same cells. When these two receptor types are stimulated simultaneously by nonselective ligands for high- and low-affinity nAChRs, they interact, bringing about an increase in binding site density of the high-affinity nAChRs.

Animals↗