Biomedical subjects
Publications and source records attributed to M Markianos.
The prolactin response after ECT in ten female melancholic patients correlated significantly to their prolactin response to i.v. TRH. These findings may suggest an underlying common mechanism between TRH and ECT regarding their PRL releasing properties.
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The serum prolactin (PRL), luteinizing hormone (LH), testosterone (T) and estradiol (E) levels were investigated in a group of male paranoid schizophrenics with delusional ideas of homosexual content, in a group of male paranoid schizophrenics without delusional ideas of homosexual content, and in a group of healthy, male heterosexual subjects. Only male paranoid schizophrenics with delusional ideas of homosexual content had significantly lower serum PRL values and significantly higher serum E levels than those of the age-matched group of normal, male heterosexual controls; also, these patients tended to have higher (though not to a statistically significant degree) serum LH and T levels than those of normal controls. Findings of this study are discussed within the framework of the possible involvement of endocrine factors in the occurrence of delusional ideas of homosexual content in male patients with paranoid schizophrenia.
The noradrenaline, dopamine and serotonin metabolites methoxyhydroxyphenylglycol (MHPG), homovanillic acid (HVA), and 5-hydroxyindoleacetic acid (5-HIAA), as well as the cyclic nucleotides c-AMP and c-GMP were estimated in urine samples of five normal volunteers. Ten control samples and two samples after cannabis use were analyzed for each volunteer. Cannabis use caused significant decreases in MHPG and c-AMP, and increases in HVA, while 5-HIAA and c-GMP excretion remained unchanged. The results indicate that cannabis use interferes with catecholaminergic mechanisms in man, decreasing the noradrenaline and increasing dopamine turnover, probably through action on presynaptic receptors.
Forty-two schizophrenic patients under chronic neuroleptic treatment (11-24 years) were studied, 20 without and 22 with tardive dyskinetic symptomatology. Blood and urine samples were collected on 3 consecutive days. Plasma prolactin (PRL) and urinary homovanillic acid (HVA) values were higher in both tardive dyskinetic and nontardive dyskinetic groups, compared to normals. The increased PRL and HVA values were not related to tardive dyskinesia but to the actual neuroleptic dose. The subgroup of patients with actual dose under 900 chlorpromazine equivalents had normal PRL values and increased HVA at low significance level compared to normals, while the subgroup with doses over 900 equivalents had highly significant (p less than 0.001) increased PRL and HVA values. Thus, the actual neuroleptic dose determines plasma PRL and urinary HVA excretion in patients chronically treated with neuroleptics.
The noradrenergic correlates 3-methoxy-4-hydroxy-phenylglycol (MHPG) in urine and dopamine-beta-hydroxylase (DBH) in plasma were estimated on 3 consecutive days in chronic schizophrenic patients under neuroleptic treatment, 20 without and 22 with tardive dyskinetic symptomatology. Compared to normals, no differences in DBH activities were found, but MHPG excretion was higher in both patient groups. Dichotomy of DBH and MHPG values according to their medians for the 42 patients revealed a higher incidence of low DBH activities and low MHPG excretion in the tardive dyskinesia group, while there were no differences in relation to low or high actual neuroleptic dose.
Six long-term cannabis users (10 - 44 years of use) were studied for four days during which cannabis smoking was followed by three days deprivation and smoking on the fourth day. Blood samples were taken at - 30, + 30 and + 120 minutes from each smoking and once in every deprivation day. Pulse rate and blood pressure were measured before each blood sample. Prolactin and dopamine-beta-hydroxylase activity were estimated in plasma. On the third deprivation day, both prolactin and dopamine-beta-hydroxylase were significantly elevated compared to the pre-smoking values, but returned to them after the second cannabis use. The mean arterial pressure followed the same course. The data suggest that cannabis use in man reduces noradrenergic and enhances dopaminergic activity, while deprivation has the opposite effect, possibly through presynaptic receptor mechanisms.
Several neurochemical parameters were estimated in plasma and urine of patients with affective disorders in the depressive phase and later in normothymia, after successful drug treatment. Significant increases were found for the activity of the enzyme dopamine-beta-hydroxylase in plasma and the concentrations of cyclic AMP in plasma and urine. No consistent changes were found for prolactin or cyclic GMP in plasma, and for methoxyhydroxyphenylgkyglycol, homovanillic acid, 5-hydroxyindoleacetic acid and cyclic GMP in urine. The major change we observed in the clinical state of the patients is thus not reflected in change in the urinary biogenic amine metabolites. Their changes were found to correlate inversely to their pretreatment values. In normothymia, high values decrease and low values increase for all three amine metabolites, indicating that antidepressives act towards a normalization of the amine turnover mechanisms.
3-methoxy-4-hydroxyphenylglycol (MHPG) and 5-hydroxyindoleacetic acid (5-HIAA) as well as homovanillic acid (HVA) and cyclic AMP were estimated in the morning urine of 41 drug-free parkinsonian patients and 25 hospitalized controls. In 29 patients, the estimations were repeated after 2 weeks treatment with L-dopa plus decarboxylase inhibitor. Drug-free patients excreted more MHPG and less 5-HIAA than controls. The difference from controls was significant for MHPG, only for the subgroup of patients with akinesia as the main symptom (P = 0.001) and for 5-HIAA only for the tremor subgroup (P = 0.03). 2 weeks treatment with L-dopa plus decarboxylase inhibitor, increased the MHPG excretion significantly only for the akinesia subgroup, where the pretreatment MHPG values were high, while there was no change in MHPG excretion in the tremor and the rigidity subgroups. The treatment caused no change in the 5-HIAA excretion in the tremor subgroup, where the pretreatment values were low, while in the rigidity and akinesia subgroups 5-HIAA excretion was significantly decreased. These results, as well as our previous results on HVA and cyclic AMP, show that there are considerable differences among the subgroups of parkinsonian patients regarding the metabolism of dopamine, noradrenaline and serotonin.
In normals, dopamine-beta-hydroxylase activity in plasma follows a circadian rhythm with maximal values at 8 a.m. and minimal at 2 a.m. This pattern does not exist in affective patients in the phase of mania or normothymia, while it is present in the depressive phase. Plasma c-AMP has its maximal concentrations in plasma at 2 p.m. and its minimal at 2 a.m. in normals. In affective patients the minimum occurs at 2 a.m., as in normals, while the maximum is shifted 6 hours earlier, at 8 a.m., independently of the phase of the illness. During the depressive phase, the circadian rhythms of dopamine-beta-hydroxylase and c-AMP in plasma are synchronized.
Plasma dopamine-beta-hydroxylase activity (DBH) was estimated in 50 drug-free Parkinson patients, 30 of whom had never been treated, in 26 patients treated chronically with L-Dopa, and in 44 controls. 22 of the drug-free patients were examined again after two weeks treatment with L-Dopa plus decarboxylase inhibitor. In disagreement with other reports, no differences were found among the groups and no change in the enzyme activity occurred after treatment, although urinary homovanillic acid increased 20 fold. Low DBH activities could not be attributed to the age of onset or duration of illness, main symptom, depression, autonomic disturbances, or duration of drug treatment. The only difference was found in patients with dementia associated to their illness, who showed low enzyme activities.
Homovanillic acid (HVA) and adenosine-3',5'-monophosphate (c-AMP) were estimated in the morning urine of 33 drug-free Parkinson patients and 25 hospitalized controls. 21 of the patients had never been treated; the mean duration of the illness was 2.6 years. Parkinson patients excreted more HVA and less c-AMP compared to the controls; it was the subgroup with tremor as the main symptom that caused this difference, while the subgroups with akinesia or rigidity as the main symptom has values not significantly different from those of the control group. 22 of the patients were studied again after 2 weeks of treatment with L-dopa + decarboxylase inhibitor. HVA excretion increased 20-fold while c-AMP excretion decreased 9% (p less 0.05). The reduction in the c-AMP excretion was observed only in the subgroups with akinesia or rigidity as the main symptom (p less 0.025), while there was no change in the tremor group where the pretreatment c-AMP was low. The results indicate a difference in the dopamine receptor sensitivities in the subgroups of the patients.
In eight male patients with alcoholic delirium concentrations of 3-methoxy-4-hydroxyphenylglycol (MHPG) and homovannilic acid (HVA) in CSF, activity of dopamine-beta-hydroxylase (DBH) and urinary excretion of noradrenaline (NA), adrenaline (A), and dopamine (DA) were measured during the delirium and a drug-free control period. MHPG concentration in CSF, excretion of NA and A as well as activity of serum DBH were significantly elevated during the delirium phase as compared to the control period. Urinary DA excretion and HVA in CSF did not show any constant changes. There was a positive correlation (r = 0.64) between DBH activity and the intensity of the delirium (as measured on the delirium rating scale). It is hypothesized that there is a relationship between alcoholic delirium and increased central noradrenergic activity.
The aim of this study was to investigate if levels of circulating cyclic guanosine monophosphate (c-GMP) alter in preconditioning. Twenty-eight rabbits were divided into four groups. In vivo hearts were preconditioned, either with 5 min (group A, n = 8) or with 1 min (group B, n = 8) ischemia, followed by 10 min reperfusion, while groups C (n = 7) and D (n = 5) had no interventions. Protection was determined by subjecting groups A, B and C (but not D) to 30 min regional ischemia which was followed (including group D) by 2 h reperfusion. Seven blood samples were collected for the assessment of circulating c-GMP at different points of time. All results were expressed in pmol/ml using radio-immunoassay and the infarcted to risk area in percent using fluorescent particles and tetrazolium chloride (TTC). Circulating c-GMP increased during long ischemia only in group A (baseline value 47 +/- 4, long ischemic values 60.5 +/- 4 and 60.4 +/- 4, p < 0.05). Circulating c-GMP in group A was significantly higher in the middle of the long ischemia in comparison to the groups B, C and D (60.5 +/- 4 vs 43.9 +/- 4, 45.8 +/- 5 and 43.6 +/- 4, p < 0.05). Infarcted to risk ratio was lower in group A than in groups B and C (12.2 +/- 4 vs 29.6 +/- 6 and 34.2 +/- 6 respectively, p < 0.05). Circulating c-GMP is increased in classically preconditioned in comparison to ineffectively preconditioned hearts or to control groups. This elevation may be related to the protective effect of this phenomenon.
Homovanillic acid (HVA), the main dopamine metabolite, and prolactin (PRL) were estimated in plasma and cerebrospinal fluid (CSF) of 11 male epileptic patients treated with antiepileptic drugs and of 14 neurologic controls. A trend toward higher concentrations in plasma and lower concentrations in CSF in the patient group as compared with controls was observed for both parameters. The plasma to CSF ratios of HVA and PRL levels were significantly higher in the patient group. This shift may be due to an influence of the drugs on the blood-brain barrier (BBB) permeability. The PRL levels in the CSF correlated negatively to the HVA levels in CSF in the patient group only.
The serotonin, dopamine, and noradrenaline metabolites 5-hydroxyindoleacetic acid (5-HIAA), homovanillic acid (HVA), and methoxyhydroxyphenylglycol (MHPG), were measured in urine of 38 male patients with idiopathic epilepsy on a single drug regime, and in 36 male healthy controls. Twenty patients were on carbamazepine and 18 on diphenylhydantoin. The concentrations of HVA and MHPG did not differ from normal, but 5-HIAA was significantly reduced in both patient groups. The reduced serotonin catabolism may be the result of a better utilisation of serotonin in the synapses, caused by the antiepileptic medication.