Biomedical subjects
V P Barkhatova
Publications and source records attributed to V P Barkhatova.
[Neurotransmitter changes in multiple sclerosis].
Elevated levels of norepinephrine and of excitatory amino acids (glutamate, aspartate) were observed in cerebrospinal fluid of patients with multiple sclerosis while there were elevated content of glutamine, asparagine and glycine in their blood. An important point concerning these results was the relation between biochemical indices and the character of neurological symptoms, their severity as well as the course of the disease. The role of neurotransmitters in pathogenesis of multiple sclerosis and particularly in biochemical mechanisms of the relation between nervous and immune system that underlie the development of neurological deficiencies is suggested.
[Neurotransmitter changes in amyotrophic lateral sclerosis].
The results of investigation concerning both total and cerebral catecholamine metabolism indices in 78 patients with amyotrophic lateral sclerosis (ALS) are presented. The considerable elevation of both blood and liquor norepinephrine level as well as of blood epinephrine concentration was observed together with acute decrease of platelet MAO B activity. The conclusion was made about the participation of catecholamines in exitotoxic mechanisms of motor neurons systems death which was quite characteristic for ALS development. A short literary review was presented concerning the role of neurotransmitters in regulation of motor functions. The neurochemical disturbances which may result in release of exitotoxic mechanisms of ALS were considered too. The consideration of data obtained as well as the analysis of modern conceptions of ALS pathogenesis enable both to determine some ways of ALS pathogenetic therapy and to define the basic directions of further investigations.
[The pathology of catecholamine metabolism in cerebrovascular diseases].
Blood catecholamines were investigated with high-performance liquid chromatography and electrochemical detection in 95 patients with cerebrovascular affections. On day 1-3 since ischemic apoplexy blood norepinephrine and dopamine levels increased significantly. This is possibly due to their active release from neurons in brain tissue ischemia. High blood catecholamines are thought an unfavourable factor aggravating the disease and responsible for cardiac sequelae. Ways of cerebral tissue protection in case of ischemia are suggested.
[Pathological status of catecholamines in the corpus striatum in hepatocerebral dystrophy (Wilson-Konovalov disease)].
The content of catecholamines in the striatum was measured in 2 patients suffering from hepatocerebral dystrophy (Wilson-Konovalov disease). It is noted that in different clinical manifestations of the disease, the changes in the content of noradrenaline in the striatum varied. A male patient with marked tremor spreading manifested a considerable rise of the content of catecholamines, primarily in the n. caudatus. At the same time in a female patient with a grave akinetic -rigid syndrome and the signs of liver failure, the content of catecholamines, particularly dopamine, in the putamen was low. In view of this fact it is assumed that disorders of cerebral metabolism of catecholamines, dopamine in particular, evidently related to deposition of excess copper, leading to the changes of their content in basal ganglia underline the clinical pleomorphism of the disease and play the key role in the development of extrapyramidal motor disturbances characteristic of hepatocerebral dystrophy.
[Catecholamine metabolism in essential tremor].
The pathogenesis of essential tremor (ET) is evidently very complicated and involves various biochemical and pathophysiological mechanisms. The pathology of cerebral adrenergic systems is attributed a high value in the development of the disease. The general catecholamine (CA) metabolic indices were investigated in 40 ET patients. CA excretion was considerably decreased, especially that of norepinephrine, while the urinary level of a CA precursor DOPA was essentially normal. The excretion of a major epinephrine and norepinephrine metabolite vanillylmandelic acid also tended to decrease. Contrarily to the CA excretion, their blood levels did not change considerably. The data are supposed to point to a reduction of the general CA body pool, especially of norepinephrine. This yields the shift of relationship between lepinephrine and norepinephrine toward the latter, that can provide another mechanism for ET. Possible deterioration of noradrenergic neurotransmission as a pathogenic factor of ET, and adrenergic receptors hypersensitivity in particular, are still pending. Major genetically predetermined biochemical defect in ET leading to impaired control of complicated mechanisms behind the regulation of synchroneous activity of spinal motor structures, is believed to be closely related to CA systems modifying ET in response to various impacts and involving the mechanisms of central action alcohol.
[Catecholamine metabolism in extrapyramidal disorders in patients with chronic hypertensive encephalopathy].
Total and cerebral metabolism of catecholamines (CA) was examined in patients with associated chronic hypertonic encephalopathy and extrapyramidal disorders. It was discovered for the first time that there was an increase in noradrenaline in the blood and cerebrospinal fluid together with a lowering of the content of dopamine and major metabolite thereof along the pathway of oxidative deamination of homovanillic acid. CA metabolism was shown to correlate with the patients' age, duration and gravity of extrapyramidal disorders. It is suggested that the revealed metabolic disorders of CA--neurotransmitters which are likely to underlie the development of neurological deficiency and characteristic mental disorders occur as a result of the diverse complex of biochemical alterations and are related both to the complex mechanisms of the pathogenesis of essential hypertension and ischemic injury to the brain as well as to the localization in the brain of lacunar infarctions. The complexity of the pathogenic treatment of the disease is emphasized. The main approaches to the pharmacological correction of the revealed disorders are outlined.
[Characteristics of biochemical, electrophysiological and morphological changes in experimental cerebral ischemia].
The results of experiments performed in Wistar rats are indicative of the catecholamine release during the first hours of developing cerebral ischemia, and their role in activation of lipid peroxidation (LP). These events were characteristically enhanced in the ischemic hemisphere where EEG changes were most pronounced. Maximal changes in slow parieto-occipital EEG waves amplitude and malonic dialdehyde levels in the brain tissue were also correlated. This metabolic-electrophysiological link than could be of major importance for EEG monitoring of brain pathochemistry and pathology needs, however, further investigation. Among pathological findings, the relationship between the degree of ischemic neuronal changes on one hand, and brain swelling and hyperemia on the another, was worth attention. The lack in distinct correlations between metabolic, electrophysiological and structural changes in the ischemic brain can be accounted for by a substantial spread of ischemic damage over the brain.
[Role of catecholamines in the pathogenesis of extrapyramidal hyperkinesis].
The total and cerebral metabolism of catecholamines was studied in 134 patients with various extrapyramidal hyperkinetic syndromes. Homovanillic acid levels determined in the ventricular and lumbar cerebrospinal fluid served as an indicator of the cerebral metabolism of dopamine. In two patients with hepatocerebral dystrophy (HCD) and torsion dystonia the author studied the content of catecholamines in the cerebral tissue. This study showed a considerable increase in noradrenalin and dopamine levels in the striatum, which was more pronounced in cases of HCD. It has been concluded on the basis of the findings obtained that elevation of cerebral dopaminergic activity is one of characteristic biochemical signs of extrapyramidal hyperkineses. There was a significant increase in this activity following the destruction of the ventrolateral nucleus of the thalamus, which appears to be one of the biochemical mechanisms underlying an unfavourable effect of stereotaxic surgery for extrapyramidal hyperkineses. The importance of this pathology of noradrenergic systems in the pathogenesis of extrapyramidal diseases remains unclear and needs further investigation.
[Determination of blood catecholamines by high performance liquid chromatography using electrochemical detection].
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[Neurotransmitters in Huntington chorea (review)].
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[Role of catecholamines in regulating motor functions (review)].
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[Homovanillic acid content in the cerebrospinal fluid as an index of dopamine cerebral metabolism before and after a stereotaxic operation in patients with extrapyramidal hyperkinetic syndromes].
The level of homovanillic acid (HVA) in the cerebrospinal fluid (CSF) as an indicator of the cerebral metabolism of dopamine was examined prior to and after the stereotaxic operation on the basal ganglia in 13 patients with extrapyramidal hyperkinetic syndromes. The HVA levels in the lumbar CSF decreased significantly (P less than 0.01) following the operation. The data obtained suggest that a decrease in the activity of the central dopaminergic systems secondary to the destruction of the ventrolateral nucleus of the thalamus affects the biochemical mechanisms underlying the therapeutic effect of stereotaxic operations on extrapyramidal hyperkineses. A possible relationship of the ventrolateral nucleus of the thalamus with dopaminergic and other neurotransmitter systems involved in the regulation of extrapyramidal motor functions is discussed. The findings obtained are important for the understanding of the role of the dopaminergic systems in the pathogenesis of extrapyramidal hyperkinetic syndromes and for the identification of the biochemical mechanisms underlying the therapeutic effect of stereotaxic operations.
[Several biochemical mechanisms of the pathogenesis of Huntington chorea].
Parameters of catecholamine and acetylcholine metabolism were investigated in 55 patients with Huntington's chorea. Heterogeneous nature of the results obtained by examining excretion of catecholamines, their precursors, and metabolites appears to reflect varying degrees of the damage to the cerebral neurotransmitter systems and their imbalance in different patients. It is suggested that the level of catecholamine metabolism in the body is genetically determined. A decrease in the homovanillic acid in the ventricular fluid is attributed to a low pool of dopamine in atrophied basal ganglia and/or hydrocephalus concomitant with Huntington's chorea. The activity of the blood cholinergic system was shown to be decreased, which suggests a generalized nature of acetylcholine metabolism disorder. The data obtained indicate that the biochemical mechanisms of the pathogenesis of Huntington's chorea are intricate in their nature and involve different neurotransmitter systems, which explains insufficient efficacy of the current conclusive methods used for controlling this disease. The development of multiple modality treatment affecting various sides of impaired metabolism of neurotransmitters seems to be promising.
[New trends in the treatment of hereditary nervous system diseases].
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[Role of catecholamines in the biochemical mechanisms of the pathogenesis of hepatocerebral dystrophy].
In 48 patients with hepatocerebral dystrophy the principal parameters of the catecholamine metabolism were examined. Pronounced changes characterized primarily by a considerable diminution of dopamine and noradrenaline excretion and an increase of the excretion of their immediate precursor, i.e. DOPA, were noted. On the basis of the data obtained it was assumed that the synthesis of these neurotransmitting catecholamines was depressed. In the course of treatment with d-penicillamine which is capable of mobilizing copper and stimulating its excretion from the body a statistically significant increase of the dopamine excretion (as compared with its initial level) was noted, and in patients with the graver rigid-arrhythmohyperkinetic form of the disease the excretion of not only dopamine, but also noradrenaline, was increased. It is supposed that the disturbances of catecholamine metabolism in hepatocerebral dystrophy have a complicated mechanism, and are associated with both the grave hepatic pathology and disturbances of copper metabolism. In this connection additional methods of treating that disease are offered. These methods influence catecholamine metabolism, and act primarily on extrapyramid motor, and also psychic disorders. The studies carried out by the author make a contribution to the existing concepts of the biochemical mechanisms of the hepatocerebral dystrophy pathogenesis, and expand the possibilities of treating the grave hereditary disease.
[Approaches to the study of dopamine metabolism in various extrapyramidal diseases].
The authors present the results of examining the content of 4-hydroxy-3-methoxy-phenylacetic or homovanillic acid (the principal end metabolite of dopamine) in the ventricular fluid of patients suffering from various extrapyramidal diseases. A considerable lowering of the homovanillic acid (HVA) concentration is demonstrated in patients with parkinsonism: this reflects the degeneration of the dopamine-containing pathways and the lowering of the dopamine synthesis in the basal ganglia in that disease. The treatment with L-DOPA leads to a considerable rise of the HVA level in the ventricular fluid, the fact, that points to an intensification of dopamine metabolism in the brain, when its precursor, i.e. L-DOPA is given to the patients. In patients with deforming muscular dystonia, statistically significant differences of the HVA concentration in the cerebrospinal fluid were noted. These differences correlated with the clinical manifestations of the disease. The concentration was found to be much higher in patients with local muscular rigidity, than in those in whose clinical picture the dystonic hyperkinesis was prevalent. It is concluded that in phenotypically different forms of the deforming muscular dystonia the character of the pathology of the central dopaminergic system is also different. Patients with Huntington's chorea showed a low level of the HVA in the intraventricular fluid. It is supposed that this is an evidence of either a fall of the dopamine total content in the brain because of the degeneration of the respective neurons, or of a deterioration of cerebral dopamine catabolism because of enzymatic insufficiency. The data obtained are of importance for understanding the pathogenesis, and for developing methods of treating extrapyramidal motor disturbances.
[Value of homovanillic acid determination in ventricular cerebrospinal fluid to assess brain dopamine metabolism in several extrapyramidal diseases].
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