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Biomedical subjects

A Agnoli

Publications and source records attributed to A Agnoli.

At least 91 records · Page 5Linked to original sources
PubMed1982

Drug action on the metabolic changes induced by acute hypoxia on synaptosomes from the cerebral cortex.

The synaptosomal fractions obtained from the motor area of the cerebral cortex of normocapnic, normoxic, or hypoxic, untreated beagle dogs and of pentobarbital (Nembutal)- or cytidine diphosphate (CDP)-choline-treated dogs were incubated and analyzed for ATP, ADP, AMP, creatine phosphate, pyruvate, and lactate. The data were compared with data obtained by the surface freezing technique from the whole contralateral cortical area. The in vivo intracarotid perfusion of the drug differentially affected the content of the metabolites and their ratio. This occurred whether the evaluations were performed in the incubated synaptosomal preparations or in whole cerebral tissue, both during normoxia and after hypoxia (15 min; PaO2 = 17-19 mm Hg). Thus, intracarotid perfusion of nembutal increased the synaptosomal phosphorylation state both in normoxic and in hypoxic animals, whereas the effect on the metabolism of the contralateral cortical motor area as a whole was in all cases less than that observed in the synaptosomal fraction. Perfusion with CDP-choline increased synaptosomal phosphorylation after the hypoxic condition, but had no effect in normoxia or on the whole cortical tissue of the motor area. The possibility of obtaining a cerebral sparing action by utilizing molecules devoid of anesthetic action is suggested.

Acute Disease↗
PubMed1982

Prolactin response to acute administration of different L-dopa plus decarboxylase inhibitors in Parkinson's disease.

Plasma prolactin (PRL) levels modifications after acute administration of L-dopa, L-dopa plus carbidopa and L-dopa plus benserazide were studied in parkinsonian patients. PRL increase after benserazide was compared with PRL response after carbidopa at the same dosage in untreated parkinsonian patients. A further study of the hyperprolactinemic effect of benserazide was performed in vitro on isolated and dispersed rat pituitary cells. The data gathered indicate that benserazide-induced hyperprolactinemia in parkinsonian patients could be due to a direct effect of the drug at the hypothalamic level and consequently to an inhibition of dopamine decarboxylation in the tuberoinfundibular dopaminergic system. It is not possible to exclude, however, that benserazide could exert its biological activity through the production of active metabolites in vivo.

Aged↗
PubMed1982

New strategies in the management of Parkinson's disease: a biological approach using a phospholipid precursor (CDP-choline).

CDP-choline, an intermediate in the phospholipid metabolic pathway supposed to improve the functionality of the dopamine (DA) system, was administered to parkinsonian patients in a double-blind cross-over study versus placebo. All patients were already treated with L-dopa + dopa decarboxylase inhibitor. Clinical evaluations were carried out using the Webster Rating Scale (WRS), the Northwestern University Disability Scale (NUDS) and a semiquantitative rating scale for tremor, rigidity and bradykinesia. CDP-choline treatment showed a significant improvement of rigidity and bradykinesia and a less important amelioration of tremor. NUDS and WRS showed a similar positive result. Comparing the results obtained by placebo, we found that the actual clinical efficacy of CDP-choline regards mainly bradykinesia and rigidity (23 and 33% improvement, respectively). The positive effect of CDP-choline on parkinsonian patients already treated with L-dopa + dopa decarboxylase inhibitor stands for a possible action on the DA receptor through an activation of the phospholipid metabolism.

Adult↗
PubMed1982

Definition and therapy of chronic cerebro-vascular diseases.

Chronic cerebro-vascular disorders could be considered in a broad sense as a large body of knowledge in which three main categories of clinical disturbances have to be be considered: 1) Pathological aging that manifest itself with light short term memory impairment associated with a mild parkinsonian symptomatology or pseudobulbar signs. 2) Senile dementia Alzheimer type and multi infarct dementia. 3) Chronic cerebro-vascular disorders as defined by the Ad Hoc Committee (Paris, 1980). At present the therapy of chronic cerebro-vascular disorders is based on two main groups of drugs and can be divided into: 1) A treatment of prevention or secondary prevention which tends to correct or modify the different risk factors. 2) A treatment that seeks to control and modify the neurological and neuropsychological after effects and the disorders of the higher nervous activities which result from the lesion.

Cerebrovascular Disorders↗
PubMed1981

Prolactin response as an index of dopaminergic receptor function in Parkinson's disease. Correlation with clinical findings and therapeutic response.

Circadian rhythms of prolactin have been evaluated in thirteen untreated parkinsonian patients before and after 15 days of treatment with L-Dopa + carbidopa. The 24th secretory pattern was not significatively different from that observed in controls. The L-Dopa + carbidopa therapy does not change the basal circadian prolactin (PRL) rhythm. These results suggest that the tubero-infundibular dopaminergic system (TIDA) and the PRL secretion are conserved in untreated parkinsonian patients (PP). During chronic L-Dopa + carbidopa therapy, the basal PRL levels, evaluated in 21 PP, showed a correlation with the severity of clinical features. The effects of single doses of apomorphine, bromocriptine, lisuride and haloperidol, were studied on serum levels of PRL in 21 PP divided in two groups of "responders" and "non-responders". Haloperidol induced an enhancement of serum PRL; the dopaminergic drugs, apomorphine, bromocriptine and lisuride inhibited basal PRL secretion. It seems that the TIDA system, in Parkinson disease is not significatively altered, even though presenting a remarkable slower response in "non-responders" to L-Dopa therapy. We also evaluated the effect of L-Dopa, L-Dopa + carbidopa, bromocriptine, lisuride, nomifensine and deprenyl on growth hormone secretion in six PP. The endocrine effects of dopaminergic drugs show a mild rise in comparison with controls suggesting an important alteration in the dopamine (DA) control of growth hormone (GH).

Adult↗
PubMed1981

[The problem of side-effects: cardiotoxicity (author's transl)].

The cardiotoxicity of tricyclics is wellknown. The interpretations of such a mechanism are many: the tricyclic ring, the dimetilaminic group, the re-uptake NA mechanisms at myocardic level. A study was designed in order to answer the question. Four antidepressant drugs (a true quadricyclic: mianserin; a tricyclic with short later chain: amineptine; two tricyclic antidepressants with long chain: amitriptyline and chlorimipramine) were chosen in the double-blind cross-over study design in two different types of depression: anxious and retarded depression. A computerized cycloergometer test was performed at different times, together with ECG and depression evaluation. The patients with retarded depression were treated with amineptine (from 150 mg to 300 mg/day) and after a wash-out periods with chlorimipramine (150 mg/day). The patients with anxious depression were treated with mianserin (30-60 mg/day) for a fortnight and afterwards with amitriptyline (150 mg/day). The evaluation of the ergometric tests carried out at the fixed day have been carried out using the "Minnesota methodology". The results obtained show that the quadricyclic (mianserin) doesn't point out any cardiotoxicity. All tricyclics, especially amitriptyline, show cardiotoxicity signs.

Amitriptyline↗
PubMed1980

Dopaminergic and non-dopaminergic neurons in substantia nigra: differential response to bromocriptine.

Bromocriptine reduces the spontaneous firing rate of neurons in the pars compacta of the substantia nigra but does not change the electrical activity of the neurons located in the pars reticulata. On the other hand, bromocriptine induces contralateral circling behaviour in rats with unilateral 6-hydroxydopamine nigral lesion. This increased motor activity follows an initial period of hypomotility. The decrease of the neuronal firing rate in the pars compacta of the substantia nigra coincides with the hypomotility observed in the lesioned rats.

Animals↗
PubMed1980

Striatal cholinergic receptors and dyskinetic motor activity in the rat.

An injection of D-tubocurarine into the rat striatum produces a complex motor syndrome resembling in part that induced by picrotoxin. The destruction of the dopaminergic terminals by 6-hydroxydopamine does not prevent these effects of D-tubocurarine on motor activity. Hence neither dopamine release nor the presynaptic acetylcholine receptors are responsible for the D-tubocurarine-induced movements. On the other hand, lesion of the striatum by kainic acid abolishes the motor abnormalities due to D-tubocurarine but not those due to picrotoxin injection. Therefore, the effects of picrotoxin might be attributable to an action on GABA receptors still present in the kainic acid-treated striatum, whereas the effects of D-tubocurarine might be due to its action on striatal postsynaptic acetylcholine receptors.

Animals↗