Cytophotometric determination of RNA in various brain structures of hypoxia-adapted and unadapted epilepsy-prone rats at different times after an epileptic seizure shows much smaller decreases in RNA levels and their much more rapid return to normal in the adapted than in the unadapted rats. The adaptation to hypoxia produces a marked anticonvulsive effect, and this effect is enhanced and prolonged considerably by pharmacotherapy.Key Words: adaptation to hypoxia; audiogenic epilepsy; therapy Adaptation to periodic hypobaric hypoxia has been shown to increase considerably the resistance of Krushinsky-Molodkina (KM) rats to audiogenic epilepsy [6][7][8][9], to which they are genetically predisposed. While it has been suggested that the activation of nucleic acid and protein syntheses and the elevation of RNA content ha the brain that occur during adaptation may play a role in the antiepileptic effect of the latter [12], the question of how an audiogenic convulsive seizure might affect RNA concentration ha neurons of various brain structures of hypoxia-adapted and unadapted animals has not been addressed. Nor is it known how long the anticonvulsive effect of adaptation is retained after a course of adaptation and whether this effect can be prolonged by pharmacological means.Accordingly, the objectives of this study were to measure RNA levels in neurons of various brain nuclei at different times after an audiogenic epiInstitute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences, Moscow leptic seizure ha hypoxia-adapted and unadapted animals, to see how rapidly the resistance to audiogenic epilepsy declines after the termination of adaptation, and to f'md out whether and to what extent the resistance can be prolonged by pharmacological agents.
MATERIALS AND METHODSThe study was conducted on male KM rats weighhag 160-180 g which all reacted to an audiogenic stimulus (an electric bell ring of 90 dB) by motor excitation that terminated in clonic convulsions. The rin~ng was stopped as soon as these were observed. Limiting the duration of acoustic stimulation prevents mortality and the development of extensive subdural hemorrhages in the rats [8,9], which makes the KM rat model a very convenient tool for evaluating the anticonvulsive effect of adaptation.Adaptation of the test rats to periodic hypoxia was achieved by elevating them to an "altitude" of
Compensated and decompensated heart failure are characterized by different associations of disorders in the brain and heart. In compensated heart failure, the blood flow in the common carotid and basilar arteries does not change. Exacerbation of heart failure leads to severe decompensation and is accompanied by a decrease in blood flow in the carotid and basilar arteries. Changes in monoamine content occurring in the brain at different stages of heart failure are determined by various factors. The functional exercise test showed unequal monoamine-synthesizing capacities of the brain in compensated and decompensated heart failure. Reduced capacity of the monoaminergic systems in decompensated heart failure probably leads to overstrain of the central regulatory mechanisms, their gradual exhaustion, and failure of the compensatory mechanisms, which contributes to progression of heart failure.
Circadian peculiarities of HR regulation and functional capacities of the heart in WAG/Rij rats with genetically determined absence epilepsy are related to spike-wave activity of the brain. The number of spike-wave discharges (SWD) is maximum at night, early morning, and evening time and decreases to minimum at 08.00-16.00. At night, functional capacities of the heart are reduced and stress test at night induces ischemic changes in the myocardium at a lower functional load than in the daytime (low level of SWD activity). The decrease in the number of SWD and spike-wave index during the daytime contributes to the central mechanisms of autonomic regulation of the heart. However, these capacities are reduced against the background of increased seizure activity during nighttime.
Многочисленные исследования болезни Паркинсона (БП) свидетельствуют, что неврологические нарушения, возникающие при прогрессирующей дегенерации дофами нергических нейронов нигростриарной системы, не ограничиваются мозгом и часто вызывают тяжелые вегетовисцеральные дисфункции, нарушая в том числе регуляцию сердечно-сосудистой системы (ССС) [1, 2]. Дегенеративные
The aim of the study was to determine the influence of pre-symptomatic and symptomatic stages of Parkinson’s disease and its treatment on the cardiac disorders in C57BL/6 mice. Materials and methods. Investigations were carried out on C57BL/6 male mice. Degeneration of dopaminergic neurons were created by the neurotoxin. In freely moving animals in online regime a 24-hour ECG recording using wireless telemetry system ML880B106 was conducted. After completing studies animals was injected L-dopa (a precursor of dopamine synthesis). All the animals underwent repeated study of HRV. Results. The disbalance of autonomic heart regulation develops already in the pre-symptomatic stage of Parkinson’s disease. The early symptomatic stage is accompanied by the aggravation of heart dysfunction due to the shift of the autonomic balance towards the increase of sympathetic and decrease of parasympathic effect on the heart. Coronary disorders concomitant to Parkinson’s disease increase a risk of life threatening arrhythmia and sudden death syndrome not only in the early symptomatic stage but also in the pre-symptomatic stage. Conclusions. L-dopa effectively restores the structure of heart rate and prevents the risk of life threatening arrhythmia only in the pre-symptomatic stage of disease.
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