scholarly journals Effect of the Organic Calcium Antagonist D-600 on Cerebrocortical Vascular and Redox Responses Evoked by Adenosine, Anoxia, and Epilepsy

1983 ◽  
Vol 3 (1) ◽  
pp. 51-61 ◽  
Author(s):  
Arisztid G. B. Kovách ◽  
Eörs Dóra ◽  
Sándor Szedlacsek ◽  
Ákos Koller
Keyword(s):  
Calcium Ions ◽  
Calcium Antagonists ◽  
Redox State ◽  
Brain Cortex ◽  
Calcium Influx ◽  
Epileptic Seizures ◽  
Metabolic Effects ◽  
Minor Role ◽  
The Brain ◽  
Nadh Redox State

The purpose of this study was to investigate the role of calcium ions in cerebrocortical vasodilatation and oxidized and reduced nicotinamide adenine dinucleotide (NAD/NADH) redox responses evoked by adenosine, anoxia, and epileptic seizures. The brain cortex of chloralose-anaesthetized cats was treated locally with gallopamil-hydrochloride (D-600) and verapamil (Isoptin®). These organic calcium antagonists decrease the inward movement of calcium ions into vascular smooth muscle cells. Cerebrocortical vascular volume (CVV) and NADH fluorescence were measured in vivo by fluororeflectometry. Adenosine and calcium antagonists were dissolved in artificial cerebrospinal fluid (mock CSF) and applied topically to the brain cortex by superfusion. Adenosine (10−8 to 10−3 M) resulted in concentration-dependent increases in CVV. The NAD/NADH redox state was not altered below adenosine concentrations of 10−5 M. However, in the concentration range of 10−5 to 10−3 M, significant NAD reduction was obtained. Both calcium antagonists increased CVV markedly, but did not bring about significant changes in NAD/NADH ratio and local electrical activity of the exposed brain cortex. D-600 (2 × 10−6 M) increased CVV as much as did 10−4 M adenosine, but it failed to diminish the vascular and metabolic effects of the adenosine. D-600 (2 × 10−4 M) resulted in an increase in CVV approximately 2.5 times greater than that caused by 10−4 M adenosine alone. However, the adenosine-induced CVV response was inhibited by only about 70%, compared with the control response. After pretreating the brain cortex with 2 × 10−3 M D-600, adenosine had no effects on CVV and NAD/NADH redox state; the NAD reduction accompanying anoxia and epileptic seizures was considerably diminished. These results suggest that the inhibition of transmembrane calcium influx could have a minor role in the vasodilatatory mechanism of adenosine. Since the vascular effect of adenosine vanished only at very high concentration of D-600, which might also inhibit the release of calcium from intracellular binding sites, it is presumed that adenosine dilates the cerebrocortical vessels by interacting with intracellular calcium-sequestrating mechanisms. Furthermore, since adenosine had a marked NAD reducing effect and since it is well known that it increases the activity of adenylate cyclase and phosphorylase enzymes, accumulation of 3′,5′-cyclic adenosine monophosphate (cAMP) and substrate mobilization might be involved also in the vasodilatatory mechanism of adenosine. Our results concerning the inhibitory effect of D-600 on epilepsy- and anoxia-induced cerebrocortical NAD reduction unambiguously demonstrate the significance of calcium fluxes in glycogen and glucose metabolism under these conditions.

Multiparametric monitoring of the awake brain exposed to carbon monoxide

1995 ◽  
Vol 78 (3) ◽  
pp. 1188-1196 ◽  
Author(s):  
A. Mayevsky ◽  
S. Meilin ◽  
G. G. Rogatsky ◽  
N. Zarchin ◽  
S. R. Thom
Keyword(s):  
Carbon Monoxide ◽  
Blood Flow ◽  
Redox State ◽  
Ionic Homeostasis ◽  
Awake Rat ◽  
Brain Oxidative Stress ◽  
The Brain ◽  
Measurable Change ◽  
Nadh Redox State

We have applied in vivo real-time techniques to monitor the physiological changes associated with exposure to a pattern of carbon monoxide (CO) known to cause brain oxidative stress. Using a multiparametric monitoring device connected to the brain, we exposed unanesthetized rats to two levels of CO, 0.1 and 0.3% in air. Energy metabolism was evaluated by the optical monitoring of relative cerebral blood flow (CBF) and intramitochondrial redox state. Ionic homeostasis was assessed by measurements of K+,Ca2+, and H+ or Na+ levels in the extracellular space. The electrical parameters monitored were the electrocorticogram and direct current steady potential. Under 1,000 ppm of CO, the CBF was increased significantly without any measurable change in the NADH redox state, suggesting that the cause for the increased CBF was not hypoxia. Exposing the awake rat to 1,000 ppm of CO (40 min) followed by 3,000 ppm of CO (20 min) led to an increase in CBF followed by episodes of spontaneous brain depolarizations characterized by changes in ionic homeostasis and blood flow. These changes were similar to those recorded under cortical spreading depression. In most animals exposed to 3,000 ppm of CO, spontaneous oscillations in CBF and NADH redox state that were negatively correlated were recorded. The results indicate that an inspired CO level of 0.1% had effects largely restricted to blood flow, whereas at a higher CO level an additional impairment in energy supply resulted in a complex pattern of effects similar to that caused by brain ischemia.

NAD/NADH: redox state changes on cat brain cortex during stimulation and hypercapnia

1982 ◽  
Vol 243 (6) ◽  
pp. H1032-r-H1032-r
Author(s):  
Laszlo Gyulai ◽  
Eörs Dora ◽  
Arisztid G. B. Kovach
Keyword(s):  
Experimental Research ◽  
Redox State ◽  
Brain Cortex ◽  
University Of Pennsylvania ◽  
Research Department ◽  
Cat Brain ◽  
State Changes ◽  
Medical University ◽  
Nadh Redox State

Page H619: Laszlo Gyulai, Eörs Dora, and Arisztid G. B. Kovach. “NAD/NADH: redox state changes on cat brain cortex during stimulation and hypercapnia.” Authors' affiliation line should read: Experimental Research Department and Second Institute of Physiology, Semmelweis Medical University, Budapest, Üllöi ut 78/a, Hungary. Address for reprint requests: L. Gyulai, Johnson Research Foundation, University of Pennsylvania, 37th and Hamilton Walk, Richards Bldg.Ü5th Floor, Philadelphia, PA 19104.

scholarly journals Effect of Topical Adenosine Deaminase Treatment on the Functional Hyperemic and Hypoxic Responses of Cerebrocortical Microcirculation

1984 ◽  
Vol 4 (3) ◽  
pp. 447-457 ◽  
Author(s):  
Eörs Dóra ◽  
Ákos Koller ◽  
Arisztid G. B. Kovách
Keyword(s):  
Electrical Stimulation ◽  
Adenosine Deaminase ◽  
Brain Cortex ◽  
Brain Activation ◽  
Epileptic Seizures ◽  
Direct Electrical Stimulation ◽  
Cyanide Poisoning ◽  
Vascular Volume ◽  
The Brain

The purpose of this study was to investigate the possible importance of adenosine in cerebrocortical vasodilatation accompanying brain activation (epileptic seizures and direct electrical stimulation) and hypoxia (arterial hypoxia and cyanide poisoning of the brain cortex). In chloralose-anesthetized cats a circumscribed area of the brain cortex was treated with adenosine deaminase (Type III; Sigma), which potently deaminates adenosine to the nonvasoactive inosine. Cerebrocortical vascular volume and fluorescence of reduced nicotinamide adenine dinucleotide were measured in vivo by surface fluororeflectometry. The responses of small pial and intracortical vessels to brain activation and hypoxia were studied in brain cortices superfused with artificial (mock) CSF and 5 U/ml adenosine deaminase. It was found that superficially applied adenosine deaminase readily diffuses onto the brain cortex. Prolonged pretreatment of the brain cortices with 0.025 U/ml adenosine deaminase eliminated almost completely the vasodilative effect of 10−7 mol/ml adenosine. The inhibitory effect of the enzyme on adenosine-induced cortical vasodilatation was specific, because 5 U/ml adenosine deaminase did not attenuate the vasodilative potency of 10−8 mol/ml 2-chloroadenosine. Adenosine deaminase (5 U/ml) pretreatment of the brain cortices did not diminish the cerebrocortical vascular volume, which increased with arterial hypoxia, topical cyanide poisoning, and direct electrical stimulation. However, it slightly decreased the vasodilative effect of epileptic seizures. On the basis of these results, it seems very unlikely that adenosine is a critical factor in the control of cerebrovascular tone during arterial hypoxia and brain activation.

scholarly journals Effect of Acute Arterial Hypo- and Hypertension on Cerebrocortical NAD/NADH Redox State and Vascular Volume

1982 ◽  
Vol 2 (2) ◽  
pp. 209-219 ◽  
Author(s):  
Eörs Dóra ◽  
Arisztid G. B. Kovách
Keyword(s):  
Redox State ◽  
Arterial Hypotension ◽  
Minor Role ◽  
Vascular Volume ◽  
Fluorescence Measurements ◽  
Arterial Blood ◽  
Nadh Fluorescence ◽  
Alpha Receptors ◽  
A Minor ◽  
Nadh Redox State

The effects of stepwise arterial hypotension (MABP: 80, 60, 40 mm Hg) and moderate arterial hypo- and hypertension (MABP: 80, 150–160 mm Hg) on cerebrocortical vascular volume and NAD/NADH redox state were studied in anaesthetized cats, The vascular volume and NADH fluorescence measurements were performed on closed skull preparations using a microscope fluororeflectometer. To determine the possible role of adrenergic alpha-receptors in the autoregulatory adjustment of cerebrocortical vascular volume, some of the animals were pretreated with intra-arterially infused phenoxybenzamine (1 mg/kg), It was found that longlasting stepwise arterial hypotension leads to a gradual increase in cerebrocortical vascular volume and NADH fluorescence, Though the cerebrocortical arteries dilatated considerably at 80 mm Hg, sustained for 30 min, the NAD/NADH redox state failed to be reoxidized but was shifted to a more reduced state. This finding suggests that some factor other than tissue hypoxia is responsible for the dilatation of cerebrocortical vessels during moderate arterial hypotension. When the arterial blood pressure was restored following stepwise arterial hypotension, the cerebrocortical vascular volume did not decrease and the NAD/NADH redox state remained reduced, showing that the autoregulatory capability of the vessels was lost and the tissue metabolism was irreversibly altered. During a 5-min duration of moderate arterial hypo- and hypertension, biphasic changes were obtained in cerebrocortical vascular volume while the NAD/NADH redox state was shifted to a more reduced and oxidized state. Since the dilatation and the constriction of the cerebrocortical vessels during arterial hypo- and hypertension lagged by 40–80 s behind the redox state alterations, it is suggested that the myogenic mechanism has a minor role in CBF autoregulation. Phenoxybenzamine (PBZ) dilatated the cerebrocortical vessels, indicating the existence of an active alpha-receptor-mediated vasoconstrictory tone. Since the extent of autoregulatory vascular volume changes was not affected by PBZ pretreatment, the involvement of adrenergic alpha-receptors in the autoregulation of CBF can be excluded, at least for cats.

scholarly journals Effect of Topically Administered Epinephrine, Norepinephrine, and Acetylcholine on Cerebrocortical Circulation and the NAD/NADH Redox State

1983 ◽  
Vol 3 (2) ◽  
pp. 161-169 ◽  
Author(s):  
Eörs Dóra ◽  
Arisztid G. B. Kovách
Keyword(s):  
Redox State ◽  
Synaptic Cleft ◽  
Nadh Oxidation ◽  
Tissue Respiration ◽  
Pial Arteries ◽  
Cranial Window ◽  
Pial Vessels ◽  
Nadh Fluorescence ◽  
The Brain ◽  
Nadh Redox State

We investigated the effects of topically administered catecholamines and acetylcholine (ACh) on the cerebrocortical microcirculation and NAD/NADH redox state in chloralose-anesthetized cats. NADH fluorescence of the brain cortex and the volume of small intracortical vessels were measured by fluororeflectometry, and in most of the experiments the pial vessels were photographed simultaneously through a cranial window. Cerebrocortical vascular volume (CVV) and the diameter of the pial vessels were decreased, and NADH was oxidized by concentrations of epinephrine and norepinephrine as low as 3 × 10−8 M. Pial veins constricted approximately twice as much as pial arteries. ACh dilatated pial arteries, slightly constricted pial veins, and increased CVV, but had no effect on the NAD/NADH redox state. Since pial and intracortical vessels were constricted markedly by catecholamines, and since these vascular reactions appeared at a lower concentration than is presumed to occur in the synaptic cleft, our results support the regulating role of these substances in cerebral circulation. NADH oxidation, obtained with catecholamines, was interpreted to be due to enhanced tissue respiration. The finding that ACh dilatated pial arteries and increased CVV, but failed to influence the NAD/NADH redox state, might indicate that the brain cortices of normal animals are bioenergetically nonhypoxic. If cortical microregions where the oxygen tension is close to zero were biochemically hypoxic, NADH oxidation should have occurred during ACh administration.

Complexity Measures of Brain Electrophysiological Activity

2010 ◽  
Vol 24 (2) ◽  
pp. 131-135 ◽  
Author(s):  
Włodzimierz Klonowski ◽  
Pawel Stepien ◽  
Robert Stepien
Keyword(s):  
Brain Activity ◽  
Deterministic Chaos ◽  
Epileptic Seizures ◽  
Eeg Signal ◽  
Eeg Signals ◽  
Complexity Measures ◽  
Electrophysiological Activity ◽  
Signal Complexity ◽  
Physiological Sleep ◽  
The Brain

Over 20 years ago, Watt and Hameroff (1987 ) suggested that consciousness may be described as a manifestation of deterministic chaos in the brain/mind. To analyze EEG-signal complexity, we used Higuchi’s fractal dimension in time domain and symbolic analysis methods. Our results of analysis of EEG-signals under anesthesia, during physiological sleep, and during epileptic seizures lead to a conclusion similar to that of Watt and Hameroff: Brain activity, measured by complexity of the EEG-signal, diminishes (becomes less chaotic) when consciousness is being “switched off”. So, consciousness may be described as a manifestation of deterministic chaos in the brain/mind.

Automated System for Epileptic Seizures Prediction based on Multi-Channel Recordings of Electrical Brain Activity

2018 ◽  
pp. 115-122 ◽  
Author(s):  
V. A. Maksimenko ◽  
A. A. Harchenko ◽  
A. Lüttjohann
Keyword(s):  
Epileptic Seizure ◽  
Brain Activity ◽  
Epileptic Seizures ◽  
Automated System ◽  
Brain Computer Interfaces ◽  
Electrical Brain Activity ◽  
Computer Interfaces ◽  
Prediction And Prevention ◽  
The Brain

Introduction: Now the great interest in studying the brain activity based on detection of oscillatory patterns on the recorded data of electrical neuronal activity (electroencephalograms) is associated with the possibility of developing brain-computer interfaces. Braincomputer interfaces are based on the real-time detection of characteristic patterns on electroencephalograms and their transformation  into commands for controlling external devices. One of the important areas of the brain-computer interfaces application is the control of the pathological activity of the brain. This is in demand for epilepsy patients, who do not respond to drug treatment.Purpose: A technique for detecting the characteristic patterns of neural activity preceding the occurrence of epileptic seizures.Results:Using multi-channel electroencephalograms, we consider the dynamics of thalamo-cortical brain network, preceded the occurrence of an epileptic seizure. We have developed technique which allows to predict the occurrence of an epileptic seizure. The technique has been implemented in a brain-computer interface, which has been tested in-vivo on the animal model of absence epilepsy.Practical relevance:The results of our study demonstrate the possibility of epileptic seizures prediction based on multichannel electroencephalograms. The obtained results can be used in the development of neurointerfaces for the prediction and prevention of seizures of various types of epilepsy in humans. 

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