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L Lima

Publications and source records attributed to L Lima.

106 records · Page 6Linked to original sources
PubMed1986

Reserpine and the monoaminergic regulation of adrenal dopamine beta-hydroxylase activity.

The systemic administration of reserpine to rats increases adrenal dopamine beta-hydroxylase activity, but is without significant effect on the Km(tyramine). This induction is partially blocked by hemisplanchnicotomy and by impairment of translation. The combined administration of (a) alpha-methyl-p-tyrosine and p-chlorophenylalanine; (b) 6-hydroxydopamine and p-chlorophenylalanine; or (c) alpha-methyl-p-tyrosine and 5,7-dihydroxytryptamine increases adrenal dopamine beta-hydroxylase activity. These results suggest that the simultaneous depletion of central serotonin and catecholamines, as achieved by reserpine alone or by conjoint action of two specific drugs, is necessary for the induction. p-Chlorophenylalanine (intraperitoneal) or 5,7-dihydroxytryptamine (intracerebroventricular or injected into the medial raphe nucleus) increases the effect of reserpine, but the use of a catecholamine-depleting agent with reserpine does not alter the increase of adrenal dopamine beta-hydroxylase obtained with reserpine alone. The potentiation by 5,7-dihydroxytryptamine is abolished by hemisplanchnicotomy, a result that demonstrates neural mediation of its effect. Although intravenous administration of 6-hydroxydopamine alone increases the activity of adrenal dopamine beta-hydroxylase, the combination of this treatment with p-chlorophenylalanine does not elevate it further, as occurs with intracerebroventricular injections; this suggests a specific role of central catecholamine depletion. The serotonin agonists 5-hydroxytryptophan, fenfluramine and 5-methoxy-N,N-dimethyltryptamine abolish the inducing effect of reserpine. This work sheds light on the action of reserpine as inducer and provides evidence for the role of monoaminergic pathways, with net inhibitory effects, that are involved in the regulation of the activity of an adrenal enzyme.

5,7-Dihydroxytryptamine↗
PubMed1986

Differential roles of raphe nuclei in the regulation of dopamine beta-hydroxylase in the adrenal gland of the rat.

The effect of reserpine on the activity of dopamine beta-hydroxylase (DBH) in the adrenal gland of the rat was determined following electrolytic lesion of the dorsal raphe nucleus (DRN) or medial raphe nucleus (MRN). In sham-operated rats, as well as in those with a lesion of the DRN, there was no significant modification of the action of reserpine on this enzyme. However, a lesion of MRN potentiated the inducing action of the drug. A specific role of MRN in the serotonergic regulation of adrenal DBH is suggested by this work.

Adrenal Glands↗
PubMed1986

Cholinergic and GABAergic regulation of dopamine beta-hydroxylase activity in the adrenal gland of the rat.

The administration of oxotremorine together with methylatropine to rats produces a dose-dependent increase of adrenal dopamine-beta-hydroxylase (DBH) activity. This effect is abolished by denervation of the gland and by cycloheximide. The Km for tyramine is not affected by the trans-synaptic induction of DBH by oxotremorine. The induction is selective, because similar treatment does not affect adrenal dopa decarboxylase or lactate dehydrogenase in the adrenal gland. The combination of 6-hydroxydopamine i.c.v. or propranolol i.p. does not alter the effect of oxotremorine on adrenal DBH. However, propranolol reduces the tremorigenic action of the muscarinic agonist. The systemic administration of p-chlorophenylalanine or the i.c.v. injection of 5,7-dihydroxytryptamine before oxotremorine treatment does not affect the increase of adrenal DBH. Progabide, gamma-aminobutyric acid, a (GABA)A and GABAB receptor agonist that effectively crosses the blood-brain barrier, reduces the effect of oxotremorine in a dose-dependent manner. Muscimol given by either of two routes, i.c.v. at a constant rate (Alzet minipump) or i.p., produces significant decreases of adrenal DBH activity and attenuates the action of oxotremorine. Denervation of the gland abolishes the effect of muscimol i.p. in decreasing adrenal DBH activity. Baclofen, a GABAB receptor agonist, has no effect by itself or does it affect the action of oxotremorine. None of these GABA agonists has any in vitro effect on adrenal DBH activity. Bicuculline, GABAA receptor antagonist, reverses the action of progabide in oxotremorine-treated rats with respect to adrenal DBH activity, partially blocks the effect of muscimol and enhances the increase obtained with oxotremorine.(ABSTRACT TRUNCATED AT 250 WORDS)

5,7-Dihydroxytryptamine↗
PubMed1983

Influence of Venezuelan equine encephalomyelitis virus on catecholamine metabolism in mouse CNS: early changes in turnover rates and content.

The influence of two strains of Venezuelan equine encephalomyelitis virus on catecholamine metabolism in the central nervous system (CNS) of the mouse was studied by the intracranial inoculation of NMRI-IVIC mice, 24 days old. Doses of 300 LD50 of the moderately virulent Pixuna strain and 10(4) LD50 of the nonvirulent TC-83 strain were used. The animals were sacrificed 4, 7, 12, and 18 days after the inoculation, and the CNS contents of dopamine, norepinephrine, and adrenaline were determined by a radioenzymatic method. The turnover of these compounds was studied with the aid of the enzymatic inhibitors pargyline and alpha-methyl tyrosine. With the Pixuna strain a decrease in the level and turnover of catecholamines was observed in all eight brain areas studied: cerebellum, pons-medulla, hypothalamus, mesencephalon, striatum, olfactory bulb-tuberculum, hippocampus, and cerebral cortex. In some regions the levels returned to normal in 12-18 days, but in the striatum, mesencephalon, hypothalamus, and olfactory bulb-tuberculum, recovery was slower and required at least 18 days after inoculation. The levels of catecholamines in the brain of mice inoculated with the nonvirulent TC-83 strain were not modified, but there was a decrease in the turnover.

Animals↗
PubMed1980

Clinical criteria for diagnosis of Machado-Joseph disease: report of a non-Azorena Portuguese family.

A Portuguese family of non-Azorean origin is described as affected by an autosomal dominant inherited ataxia resembling Machado-Joseph disease. Clinical criteria for diagnosis are proposed, based on a complex clinical picture extending from extrapyramidal signs to peripheral amyotrophy associated with secondary, but more specific, minor features such as progressive external ophthalmoplegia, dystonia, intention fasciculation-like movements of facial and lingual muscles, and bulging eyes. Machado-Joseph disease may be more widespread than previously believed.

Adult↗
PubMedDate not supplied

Effect of corticotropin-releasing factor on adrenal DBH and PNMT activity.

The continuous administration of CRF (corticotropin-releasing factor) by the intraventricular route, 100 ng/day, to rats over a period of 7 days, results in significant increases of DBH (dopamine beta-hydroxylase) and PNMT (phenethanol N-methyltransferase) activities in the adrenal glands. The pattern of increase in DBH response to various doses of CRF does not correspond to the effects observed on plasma corticosterone, a result that suggests that CRF is acting to increase the adrenal enzyme by means other than through the pituitary-adrenal axis. In contrast, PNMT responds to CRF in a manner indicating a correlation with glucocorticoid availability. Moreover, PNMT induction by CRF persists even after adrenal denervation; it also occurs when CRF is given subcutaneously for 3 days, in a dose of 60 ng/day. Injection of reserpine did not potentiate the effect of intraventricularly administered CRF.

Adrenal Glands↗
PubMedDate not supplied

Testosterone and GHRH gene expression in adult and old rats.

The effect of castration and testosterone replacement on GHRH gene expression was evaluated in adult male rats. Castration for 21 days did not affect GHRH mRNA levels, and also ineffective in this context was acute or chronic administration of testosterone to castrated rats. Hypothalamic GHRH mRNA was significantly reduced in aged male rats, but restoration of plasma testosterone concentrations via implanted capsules did not modify the low levels of GHRH mRNA. All in all, these findings support the notion that in adult and aged male rats GHRH-producing structures are insensitive to androgens.

Aging↗
PubMedDate not supplied

Minimally invasive coronary surgery with thoracoscopic internal mammary artery dissection: surgical technique.

BACKGROUND: We describe our technique of revascularization of the left anterior descending artery (LAD), using the left internal mammary artery (LIMA) without cardio- pulmonary bypass (CPB), by means of a 4-cm left thoracotomy and video-thoracoscopic harvesting of the LIMA. METHODS: The patient is placed in a semioblique position. The LIMA is harvested under thoracoscopic guidance. Trocars are introduced via three thoracic incisions of less than 15 mm at the level of the fourth and seventh intercostal spaces. Perforating arterial branches are cauterized or clipped. This approach allows complete dissection of the LIMA from the subclavian artery to the fifth intercostal space. A 4-cm left anterior thoracotomy is then made along the fourth or the fifth intercostal space. Rib excision is not necessary for LAD exposure. Coronary artery control is obtained with looping sutures (4/0 prolene) placed proximally and distally to the site of the anastomosis. Anastomosis is then performed with 8/0 prolene on the beating heart, under direct vision, without CPB. RESULTS: Between September 1995 and May 1996, this procedure was performed on 20 consecutive patients under age 80. There were no operative complications. The mean duration of hospitalization was six days. CONCLUSIONS: This new procedure enlarges the field of minimally invasive coronary artery bypass grafting techniques.

Dissection↗
PubMedDate not supplied

Lamotrigine as add-on therapy in treatment-resistant epilepsy. Portuguese Lamotrigine as Add-on Therapy in Treatment-resistant Epilepsy Study Group.

The efficacy and safety of lamotrigine as add-on therapy in treatment-resistant epilepsy were evaluated in an open prospective study carried out at five centres in Portugal and involving 61 patients. Daily seizure diaries were kept by patients, and used by the investigators to give a rating of response to therapy. Assessments were recorded after 1, 2, 3, 6, 9, 12, 18 and 24 months. Overall, seizure control was improved in 57% of patients, remained unchanged in 34% and deteriorated in 9%. There were some indications that efficacy was greatest in patients with generalized seizures and in those taking concomitant valproate. Efficacy was maintained throughout the 2-year study. It was possible to reduce the dose of concomitant antiepileptic drug in 56% of patients, and seven patients no longer needed a concomitant antiepileptic drug. Although 75% of patients reported an adverse experience, most of these were mild or moderate in intensity, did not require treatment and were not judged to be serious. A total of 13 patients withdrew from the study (four due to adverse events, four due to lack of efficacy and five for other reasons).

Administration, Oral↗
PubMedDate not supplied

[Central serotonin receptors and chronic treatment with selective serotonin reuptake inhibitors in the rat: comparative effects of fluoxetine and paroxetine].

The hypothesis that a dysfunction of serotonergic neurotransmission is implicated in depression is supported by the clinical efficiency of selective serotonin (5-hydroxytryptamine, 5-HT) reuptake inhibitors (SSRIs) in the treatment of depressive disorders. These drugs, such as fluoxetine and paroxetine, exert their antidepressant activity by increasing 5-HT concentration in the synaptic cleft and thus enhancing serotonergic neurotransmission. However, two to three weeks of treatment are necessary to see the first signs of clinical efficiency. Several hypothetical mechanisms have been put forward to account for this delay, taking into account pharmacokinetic considerations, neurotransmitter metabolism, and/or adaptive regulation of pre and/or post-synaptic receptors. The aim of this study was to look for such adaptive changes in the course of a 3-week treatment with fluoxetine (5 mg/kg/day, i.p.) or paroxetine (5 mg/kg/day, i.p.) in adult rats. In vitro binding and quantitative autoradiographic studies showed that neither 5-HT1A, 5-HT1B, 5-HT2A, nor 5-HT3 receptor binding sites in various brain areas were affected by these treatments. Furthermore, comparison of the specific binding of [3H]8-OH-DPAT to 5-HT1A receptors functionally coupled to G proteins with that of [3H]WAY 100635 to all 5-HT1A receptor binding sites (i.e. coupled and uncoupled with regard to G proteins) revealed no significant change in rats treated with either SSRI. Accordingly, the proportion of functional 5-HT1A receptors (i.e. those physically coupled to G proteins) appeared to remain unaltered all along a 3-week treatment with either fluoxetine or paroxetine. Nevertheless, in vitro electrophysiological recordings of serotonergic neurons in the dorsal raphe nucleus allowed the demonstration of a clearcut functional desensitization of somatodendritic 5-HT1A autoreceptors. Thus, the potency of the 5-HT1A autoreceptor agonist, 8-OH-DPAT, to depress the firing of serotonergic neurons in brain stem slices was significantly reduced as soon as after a 3-day treatment with either SSRI. The proportion of recorded neurons showing desensitization of somatodendritic 5-HT1A autoreceptors then increased along the treatment, and was generally larger with fluoxetine than with paroxetine. As 5-HT1A autoreceptor desensitization can contribute to facilitate serotoninergic neurotransmission, the remarkable efficiency of fluoxetine to trigger this adaptive regulatory mechanism might account, at least partly, for its potent antidepressant activity.

Animals↗