Bloqueantes adrenérgicos y funcionalismo tiroideo

La participación del sistema adrenérgico en las manifestaciones clínicas del hipertiroidismo, ha sido señalada por di­versos autores (GOETSCHE, 1918; PRIESTLY y cols., 1931; ROSEN­BLUM y cols., 1933; SAWYER y BROWN, 1935; McDONAL y cols., 1935; BARKER y cols., 1936; SCHNECKLOTH y cols., 1953; BREWSTER, 1956; WURTMAN y cols., 1963; GOLDSTEIN y KILLIP, 1965; HARRISON, 1967; MORI, 1968; WADA, 1968). La primera sugerencia se debe a GOETSCHE (1918 ). Este autor observó que los efectos cardíacos de la adrenalina, en pacientes hipertiroideos, estaban aumentados, mientras que, en otros procesos que cursan con taquicardia -ansiedad- el aumento era menor..

Acció de l'hormona alliberadora de la Tirotropina (TRH) damunt mecanismes andrenèrgics

Des de fa uns quants anys hom sospitava l'existencia de substàncies d'origen hipotalàmic amb acció reguladora de les secrecions anterohipo­fisàries; convencionalment eren denominades «factor d'alliberació» (re­leasing factors). Generalment hom substituïa el terme «factor» pel d'«hormona» tan aviat com aconseguia de determinar-ne l'estructura química. Aquest és el cas de l'hormona alliberadora de la tirotropina hipofisària (TRH: thyrotropin-releasing hormone), coneguda abans com a factor alliberador de la tirotropina (TRF: thyrorropin-releasing factor)

Reduced antioxidant defense in early onset first-episode psychosis: a case-control study

Background:Our objective is to determine the activity of the antioxidant defense system at admission in patients with early onset first psychotic episodes compared with a control group. Methods: Total antioxidant status (TAS) and lipid peroxidation (LOOH) were determined in plasma. Enzyme activities and total glutathione levels were determined in erythrocytes in 102 children and adolescents with a first psychotic episode and 98 healthy controls. Results: A decrease in antioxidant defense was found in patients, measured as decreased TAS and glutathione levels. Lipid damage (LOOH) and glutathione peroxidase activity was higher in patients than controls. Our study shows a decrease in the antioxidant defense system in early onset first episode psychotic patients. Conclusions: Glutathione deficit seems to be implicated in psychosis, and may be an important indirect biomarker of oxidative stress in early-onset schizophrenia. Oxidative damage is present in these patients, and may contribute to its pathophysiology

Involvement of 5-HT1A/1B receptors in the antinociceptive effect of paracetamol in the rat formalin test

The mechanism of analgesic action of paracetamol (acetominophen) remains still unknown. However, a relationship between serotonergic system and the effect of paracetamol has been previously demonstrated. The serotonin activity in the brainstem is primarily under the control of 5-HT1A somatodendritic receptors, although some data also suggest the involvement of 5-HT1B receptors. To determine whether the 5-HT1A and 5-HT1B receptors are involved in the antinociceptive effect of paracetamol, we evaluated the effect of paracetamol (0.125–1 g/kg i.p.) followed by different antagonists [WAY 100,635 (0.8 mg/kg s.c.) and SB 216,641 (0.8 mg/kg s.c.)] or agonists [8-OH-DPAT (0.125 mg/kg s.c.) and CP 93,129 (0.125 mg/kg s.c.)] of 5-HT1A and 5-HT1B receptors, respectively, in the rat model of formalin-induced pain. We demonstrated that paracetamol administration showed a dose-dependent antinociceptive effect in the formalin test. WAY 100,635 (5-HT1A antagonist) induced an increase in the antinociceptive effect of paracetamol at 250 mg/kg doses. Conversely, 8-OH-DPAT (5-HT1A agonist) decreased the antinociceptive effect of paracetamol at 500–1000 mg/kg doses. However, SB216641 (5-HT1B antagonist) modified weakly the antinociceptive effect of paracetamol at 250 mg/kg doses and CP 93,129 (5-HT1B agonist) not produce a clear effect in the antinociceptive effect of paracetamol. These results suggest that the antinociceptive effect of paracetamol can be enhanced mainly by compounds having 5-HT1A antagonist properties in the formalin test and maybe by 5-HT1B receptors antagonists. Keywords: Paracetamol, Formalin test, 5-HT1A receptors, 5-HT1B receptors, Antinociceptive effec