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Biomedical subjects

P S Papavasiliou

Publications and source records attributed to P S Papavasiliou.

At least 19 recordsLinked to original sources
PubMed1985

Selective disturbances of serum mineral profiles by electroconvulsive therapy.

In nine patients with severe affective illness, the serum profiles of Mn, Zn, Cu, Mg, and Ca before and following successful bitemporal electroconvulsive therapy (ECT) were investigated. No elemental baseline abnormalities were detected before ECT. Both high and low level electric stimulation failed to produce changes in the serum concentrations of Mg as a function of time after ECT. Group mean concentrations of Zn, Cu, and Ca decreased after ECT, but values did not reach statistical significance. In contrast high level, but not low level, stimulation was accompanied by significant brief elevation of Mn (65%, p less than .02) followed by a progressive drop below basal levels (67%, p less than .001) 2 hours post-ECT. Similar patterns were observed during the middle and last ECT. Pre-ECT baseline Mn concentrations declined by about 44% (p less than .01) after the last ECT administration. The time course of these changes, in conjunction with evidence obtained from animal experimentation, suggests that high level ECT, irrespective of the onset of antidepressant effects, may alter extracellular Mn and consequently its normal intracellular composition as a result of the sudden increase in energy expenditure imposed by convulsive activity. Possible interactions between this element and other metabolic pathways are discussed. These changes may originate from elemental participation in restorative homeostatic metabolic processes during and after ECT.

Adult↗
PubMed1983

Generalized seizures alter the cerebral and peripheral metabolism of essential metals in mice.

The effects of seizures on the cerebral and peripheral metabolism of essential metals were studied in mice. Acute and chronic seizures were produced either by electroshock (ES) or by a systemic convulsant. Organ and subcellular distribution of 54Mn and 65Zn were determined prior to and at different intervals after seizure cessation. In mice shocked for 21 days, the concentrations of manganese, zinc, magnesium, and copper were determined in selected tissues. Sham-seizured mice served as controls. When 54Mn was injected after a single ES, the isotope's retention increased in the liver by 67% (P less than 0.01) and decreased in the brain and carcass by 53 and 42%, respectively (P less than 0.01). Repeated ES further augmented these effects (P less than 0.01). These changes diminished as a function of time to the animal's recovery from ES. Liver and regional brain fractionations revealed significant perturbation in the intercellular partition of 54Mn, suggesting increased metal utilization. Brain and liver 65Zn were not affected by ES. Manganese content increased in the liver by 67% (P less than 0.01) and decreased in whole brain by 16.5% (P less than 0.01), after chronic ES. Cortical manganese and hypothalamic magnesium were the principal sites of loss. Small (12 to 13%), but significant elevations of magnesium were found in liver and skeletal muscle (P less than 0.05). Copper increased in muscle by 26% (P less than 0.02). Seizures selectively altered the normal brain and extracerebral distribution of essential metals which may lead to regional metal deficiency or excess. These changes were linked to the metabolic consequences of convulsive activity and may be relevant to seizure control and electroshock therapy in man.

Animals↗
PubMed1979

Administration of human somatotropin in levodopa-treated patients with Parkinsonism.

To investigate further the role of growth hormone (GH) on the cerebral effects of levodopa, human somatotropin (human growth hormone) was administered to four patients with parkinsonism with varying response to chronic levodopa therapy. The doses of somatotropin (5 IU) were administered on alternate days for four days, and the effects of this hormone on the patient's symptomatic control, dyskinesia, plasma GH, and dopa levels were evaluated and compared with those of patients receiving saline injections. We have demonstrated that administration of exogenous human somatotropin, even during marked and sustained elevations of plasma GH levels, does not alter the therapeutic or side effects of levodopa therapy. With one exception, plasma dopa levels after human somatotropin administration remained unchanged. We conclude that neither the endogenous increases of GH in response to levodopa nor those attained following human somatotropin administration modify in any consistent way the therapeutic and side effects of chronic levodopa therapy, and that the episodic releases of GH in response to levodopa occur independently of its cerebral effects.

Aged↗
PubMed1979

Plasma DOPA and growth hormone in parkinsonism: oscillations in symptoms.

In 19 patients with Parkinson disease, we studied the relationship of the therapeutic effect of levodopa, or dyskinesia, to the plasma content of DOPA and growth hormone (GH). Those with stable responses to levodopa, individually or as a group, showed stable and lower plasma DOPA levels than those with unstable symptomatic responses. These results show that stable and oscillating clinical responses in Parkinson disease parallel plasma DOPA levels, suggesting that there are different mechanisms in peripheral levodopa metabolism and that extracerebral mechanisms are important in regulating the availability of levodopa to the brain. Plasma GH did not differ in the two groups, suggesting that the secretion of GH is independent of the effects of levodopa in parkinsonism.

Aged↗
PubMed1978

Treatment of parkinsonism with N-n-propyl norapomorphine and levodopa (with or without carbidopa).

The effects of the concomitant administration of N-n-propyl norapomorphine (NPA) and levodopa, with and without carbidopa, were studied in 12 patients with unsatisfactory symptom control. Double-blind evaluation of the effects of NPA with suboptimal doses of levodopa or levodopa plus carbidopa (Sinemet) showed a mean overall improvement of 44% (20% to 74%) in nine patients and improvement of the "on-off" effect in five. Dyskinesia diminished in some patients after diminution of basal medication. In three patients, plasma dopa and growth hormone patterns did not differ substantially with and without NPA. The magnitude and timing of the therapeutic and side effects did not correlate with the pattern of growth hormone secretion, which suggests that this hormone might not be instrumental in the induction of these effects. N-n-propyl norapomorphine is a useful adjunct in the long-term management of patients with unsatisfactory response to levodopa.

Aged↗
PubMed1977

Levodopa, fertility, and longevity.

High concentrations of the dopaminergic drug levodopa (L-dopa, L-3,4-dihydroxphenylalanine) administered to mice in their diet affected fertility to a moderate degree and prolonged the mean life-span by a maximum of 50 percent.

Animals↗
PubMed1977

Antagonism by piperidine of levodopa effects in Parkinson disease.

The nicotinic cholinergic amine piperidine diminished both the dyskinesia and the symptomatic control in some patients with Parkinson disease receiving levodopa. Since the piperdine configuration is contained in the molecules of the apomorphine and N-propylnoraporphine, it might be responsible for the antagonism of these drugs to some effects of levodopa in Parkinson disease and for the palliation by apomorphine of some dopamine-mediated symptoms in other extrapyramidal disorders.

Aged↗
PubMed1976

Treatment of Parkinson's disease with aporphines. Possible role of growth hormone.

To avoid the main drawbacks of prolonged treatment with levodopa (involuntary movements and the "on-off" phenomenon), we administered apomorphine by mouth to 14 patients with Parkinson's disease. This treatment caused azotemia, which we circumvented by switching to N-propylnoraporpine, whose nephrotoxic dose (80 mg six times per day) was larger than its therapeutic dose (10 to 15 mg six times per day). Slowly increasing doses induced significant improvement (P less than 0.005) in all 24 patients studied, transitory mental aberrations in seven, and release of growth hormone in three patients tested. In patients previously on prolonged levodopa administration, the dyskinesia and "on-off" phenomenon were almost identical with N-propylnoraporphine, but both drawbacks were reduced or abolished in six patients by coadministration of alpha-methyldopa hydrazine plus levodopa. This coadministration seemed to abolish tachyphylaxis. We conclude that N-propylnoraporphine is very useful in the treatment of Parkinson's disease.

Administration, Oral↗
PubMed1975

Diphenylhydantoin. Blocking of levodopa effects.

Diphenylhydantoin (DPH) diminished the therapeutic effects of levodopa both in patients with parkinsonism and in patients with chronic manganese poisoning, as well as the levodopa-dependent dyskinesia for which the former were selected. In patients with Huntington chorea, it enhanced chorea and mental agitation and, thus, failed to conform with the postulated pharmacological reciprocity between Parkinson disease and Huntington chorea. These findings are in agreement with experiments done in animals in which DPH blocked a neuronal response to dopamine.

Adult↗