Determinants of brain activation-induced cortical NAD/NADH responses in vivo

Dóra, E.; Gyulai, Laszlo; Kovách, A. G. B.

doi:10.1016/0006-8993(84)90788-1

Cited by 47 publications

(21 citation statements)

References 21 publications

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“…These data contrast with data by Dora et al (1984) that NAD became reduced during neuronal activation in nor moxia. These latter investigators suggested that this NAD reduction was due to a relative increase in availability of reducing equivalents.…”

Section: Discussioncontrasting

confidence: 99%

“…The consistent presence of an oxidation peak at 605 nm demonstrated that oxida tion of cytochrome a,a3 can be recorded in intact, normoxic brain, despite the presence of hemo globin in the optical field. Since NAD and cy tochrome a,a3 redox activities were altered by hyp oxia in a similar manner (LaManna et al, 1984), then differences observed by Dora et al (1984) re main unexplained but suggest complications due ei ther to hypoxia or to light scattering.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Potassium Ion Homeostasis and Mitochondrial Redox Activity in Brain: Relative Changes as Indicators of Hypoxia

Milito

Raffin

Rosenthal

et al. 1988

J Cereb Blood Flow Metab

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Summary: This study was directed at relating ion trans port and mitochondrial redox activity during hypoxia, as a step toward definition of brain oxygen sufficiency. To accomplish this, extracellular potassium ion activity (K+o) was recorded by ion-selective microelectrodes while reduction/oxidation (redox) ratios of cytochrome oxidase (cytochrome a,a3) were monitored by reflection spectrophotometry in cerebral cortex of rats anesthetized with pentobarbital. In normoxia, neuronal activation by direct cortical stimulation produced transient oxidation of cytochrome a,a3 and elevation of K +0. Moderate hyp oxia (Pao2 above 50 mm Hg) resulted in reduction of cy tochrome a,a3 but only slight elevation of K +0. At this level of hypoxia, cytochrome a,a3 continued to respond to neuronal activation with transient shifts toward oxida tion and rates of K + 0 reaccumulation were unchanged from control. When Pao2 was further decreased below a critical threshold, stimulus-provoked oxidative responsesMaintenance of brain oxygenation is critical for normal function, ion homeostasis, and cell survival. Early consequences of brain anoxia include rapid reduction of the mitochondrial electron carriers, depression of synaptic transmission, loss of EEG activity and consciousness, and a slow increase in extracellular potassium ion activity (K +0). Subse quent to these changes, a K + 0 threshold is reached at which there are large increases in membrane conductances, maximal K + efflux, and anoxic de polarization (e.g., Chance et aI., 1962; Vyskocil et aI., 1972;Siesj6, 1978;Blass and Gibson, 1979;Hansen, 1985). 155of mitochondrial reactants were replaced by shifts toward reduction, but rates of reaccumulation of K + , spilled into the extracellular space by neuronal activation, remained unchanged. Only during severe hypoxia (Pao2 less than 20 mm Hg) was it possible in some animals to record a slowing in the reaccumulation of K + 0 without provoca tion of spreading cortical depression. These data indicate that ion transport activity in cerebral cortex is more re fractory to hypoxia than is mitochondrial redox func tioning. They suggest an in vivo parallel to the "cushion ing" effect of mitochondria in vitro, in which oxygen consumption remains constant despite fluctuations in ox ygenation and redox ratios, and also that there may be a greater anaerobic capacity to provide energy for ion transport in mammalian brain than has previously been appreciated. K ey Words: Brain oxygenation-Cy tochrome oxidase-Hypoxia-Mitochondria-Potas sium -Spectrophotometry.It remains difficult, however, to define brain ox ygen sufficiency in physiological terms. In part, this is due to the difficulty in extrapolating effects of anoxia to those produced by hypoxia because anoxia-induced changes occur so rapidly and be cause hypoxia-induced alterations do not reach maxima. Also, little is known of the relationships between brain metabolism and ion transport during hypoxia since high-energy intermediates are rela tively unchanged, at least by mild hypoxia (Si...

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Potassium Ion Homeostasis and Mitochondrial Redox Activity in Brain: Relative Changes as Indicators of Hypoxia

Milito

Raffin

Rosenthal

et al. 1988

J Cereb Blood Flow Metab

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“…The connection between the concentration of K ϩ and the decrease in mitochondrial NADH was shown in cat hippocampus (192). The effect of seizures on mitochondrial NADH was investigated later on by other groups, mainly in cat models (66,69,100,131,143,220,226,236,253,254). Vern et al (253) showed that epileptic activity, induced in hypotensive cats, caused an increase in NADH instead of a decrease.…”

Section: Responses To Energy Consumption Changesmentioning

confidence: 99%

“…Several works have been published by Chance and collaborators (96,97), in addition to those done in collaboration with Mayevsky. Dora's group published two papers in this field (69,129). Rosenthal and Martel (214) showed that ischemia affected the response to CSD, namely, instead of NADH oxidation, an increase in NADH was recorded (see also Fig.…”

Section: Responses To Energy Consumption Changesmentioning

confidence: 99%

Mitochondrial function in vivo evaluated by NADH fluorescence: from animal models to human studies

Mayevsky¹,

Rogatsky²

2007

American Journal of Physiology-Cell Physiology

320

290

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Mayevsky A, Rogatsky GG. Mitochondrial function in vivo evaluated by NADH fluorescence: from animal models to human studies. Am J Physiol Cell Physiol 292: C615-C640, 2007. First published August 30, 2006; doi:10.1152/ajpcell.00249.2006.-Normal mitochondrial function is a critical factor in maintaining cellular homeostasis in various organs of the body. Due to the involvement of mitochondrial dysfunction in many pathological states, the real-time in vivo monitoring of the mitochondrial metabolic state is crucially important. This type of monitoring in animal models as well as in patients provides real-time data that can help interpret experimental results or optimize patient treatment. The goals of the present review are the following: 1) to provide an historical overview of NADH fluorescence monitoring and its physiological significance; 2) to present the solid scientific ground underlying NADH fluorescence measurements based on published materials; 3) to provide the reader with basic information on the methodologies used in the past and the current state of the art fluorometers; and 4) to clarify the various factors affecting monitored signals, including artifacts. The large numbers of publications by different groups testify to the valuable information gathered in various experimental conditions. The monitoring of NADH levels in the tissue provides the most important information on the metabolic state of the mitochondria in terms of energy production and intracellular oxygen levels. Although NADH signals are not calibrated in absolute units, their trend monitoring is important for the interpretation of physiological or pathological situations. To understand tissue function better, the multiparametric approach has been developed where NADH serves as the key parameter. The development of new light sources in UV and visible spectra has led to the development of small compact units applicable in clinical conditions for better diagnosis of patients.real-time tissue viability; tissue spectroscopy; patient monitoring UNDERSTANDING THE MITOCHONDRIAL function has been a challenge for many investigators, including cytologists, biochemists, and physiologists, since its discovery more than 120 years ago. In addition to many books regarding the mitochondria, Ernster and Schatz (79) reviewed the history of mitochondrial structure and function studies. In the past two decades, several studies have reported mitochondrial involvement in pathological processes such as stroke (225) or cytoprotection (77). Most of the information on the mitochondrial function has been accumulated from in vitro studies. A relatively small portion of published papers dealt with the monitoring of mitochondrial function in vivo and in real time. Presently, examination of the involvement of the mitochondrial function in many pathological states, such as sepsis, requires monitoring of patients treated in intensive care units. Unfortunately, real-time monitoring of the mitochondrial function in patients has rarely been performed. The current study pres...

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“…[49][50][51] Most of the published material in this field of in vivo NADH monitoring of tissues used the subtraction of the reflectance signal (366 nm) from that of the NADH fluorescence signal measured to provide the corrected fluorescence signal. 52,53 A few attempts were made in order to improve the correction technique, but no significant improvement was found. In addition, the various correction techniques were listed and discussed in detail in Ince et al 54 Most of the published material was based on a 1:1 ratio, when subtracting the 366-nm reflectance from the 450-nm fluorescence signal.…”

Section: Monitoring Of Nadh: History Principles and Basic Technologymentioning

confidence: 99%

Mitochondrial function and tissue vitality: bench-to-bedside real-time optical monitoring system

et al. 2011

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Abstract. Background: The involvement of mitochondria in pathological states, such as neurodegenerative diseases, sepsis, stroke, and cancer, are well documented. Monitoring of nicotinamide adenine dinucleotide (NADH) fluorescence in vivo as an intracellular oxygen indicator was established in 1950 to 1970 by Britton Chance and collaborators. We use a multiparametric monitoring system enabling assessment of tissue vitality. In order to use this technology in clinical practice, the commercial developed device, the CritiView (CRV), is tested in animal models as well as in patients. Methods and Results: The new CRV enables the optical monitoring of four different parameters, representing the energy balance of various tissues in vivo. Mitochondrial NADH is measured by surface fluorometry/reflectometry. In addition, tissue microcirculatory blood flow, tissue reflectance and oxygenation are measured as well. The device is tested both in vitro and in vivo in a small animal model and in preliminary clinical trials in patients undergoing vascular or open heart surgery. In patients, the monitoring is started immediately after the insertion of a three-way Foley catheter (urine collection) to the patient and is stopped when the patient is discharged from the operating room. The results show that monitoring the urethral wall vitality provides information in correlation to the surgical procedure performed. C 2011 Society of Photo-Optical Instrumentation Engineers (SPIE).

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Determinants of brain activation-induced cortical NAD/NADH responses in vivo

Cited by 47 publications

References 21 publications

Potassium Ion Homeostasis and Mitochondrial Redox Activity in Brain: Relative Changes as Indicators of Hypoxia

Potassium Ion Homeostasis and Mitochondrial Redox Activity in Brain: Relative Changes as Indicators of Hypoxia

Mitochondrial function in vivo evaluated by NADH fluorescence: from animal models to human studies

Mitochondrial function and tissue vitality: bench-to-bedside real-time optical monitoring system

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