Effect of ?flow anoxia? and ?non flow anoxia? on the NAD/NADH redox state of the intact brain cortex of the cat

1985 ◽  
Vol 405 (2) ◽  
pp. 148-154 ◽  
Author(s):  
E�rs D�ra
Keyword(s):  
Redox State ◽  
Brain Cortex ◽  
Intact Brain ◽  
Nadh Redox State

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 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.

scholarly journals Circadian Oscillations of NADH Redox State Using a Heterologous Metabolic Sensor in Mammalian Cells

2016 ◽  
Vol 291 (46) ◽  
pp. 23906-23914 ◽  
Author(s):  
Guocun Huang ◽  
Yunfeng Zhang ◽  
Yongli Shan ◽  
Shuzhang Yang ◽  
Yogarany Chelliah ◽  
...  
Keyword(s):  
Mammalian Cells ◽  
Redox State ◽  
Metabolic Sensor ◽  
Nadh Redox State

In vivo monitoring of cellular energy metabolism using SoNar, a highly responsive sensor for NAD+/NADH redox state

2016 ◽  
Vol 11 (8) ◽  
pp. 1345-1359 ◽  
Author(s):  
Yuzheng Zhao ◽  
Aoxue Wang ◽  
Yejun Zou ◽  
Ni Su ◽  
Joseph Loscalzo ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Redox State ◽  
Cellular Energy ◽  
In Vivo Monitoring ◽  
Cellular Energy Metabolism ◽  
Nadh Redox State

scholarly journals Mitochondrial NAD+/NADH Redox State and Diabetic Cardiomyopathy

2019 ◽  
Vol 30 (3) ◽  
pp. 375-398 ◽  
Author(s):  
Jessica M. Berthiaume ◽  
Jacob G. Kurdys ◽  
Danina M. Muntean ◽  
Mariana G. Rosca
Keyword(s):  
Diabetic Cardiomyopathy ◽  
Redox State ◽  
Nadh Redox State

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.

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