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Responses to Cortical Spreading Depression under Oxygen Deficiency.

Sonn J, Mayevsky A - Open Neurol J (2012)

Bottom Line: CSD under the 3 pathological conditions caused an initial increase in NADH and a further decrease in CBF during the first phase of CSD, indicating an imbalance between oxygen supply and demand as a result of the increase in oxygen requirements.The special design of the MPA enabled identifying differences in the simultaneous responses of the measured parameters, which may indicate changes in the interrelation between oxygen demand, oxygen supply and oxygen balance during CSD propagation, under the conditions tested. 6.In conclusion, brain oxygenation was found to be a critical factor in the responses of the brain to CSD.

View Article: PubMed Central - PubMed

Affiliation: The Mina & Everard Goodman, Faculty of Life Sciences and Leslie and Susan Gonda Multidisciplinary Brain Research Center, Bar-Ilan University RAMAT-GAN 52900, Israel.

ABSTRACT

Objectives: The effect of cortical spreading depression (CSD) on extracellular K(+) concentrations ([K(+)](e)), cerebral blood flow (CBF), mitochondrial NADH redox state and direct current (DC) potential was studied during normoxia and three pathological conditions: hypoxia, after NOS inhibition by L-NAME and partial ischemia.

Methods: A SPECIAL DEVICE (MPA) WAS USED FOR MONITORING CSD WAVE PROPAGATION, CONTAINING: mitochondrial NADH redox state and reflected light, by a fluorometry technique; DC potential by Ag/AgCl electrodes; CBF by laser Doppler flowmetry; and [K(+)](e) by a mini-electrode.

Results and discussion: CSD under the 3 pathological conditions caused an initial increase in NADH and a further decrease in CBF during the first phase of CSD, indicating an imbalance between oxygen supply and demand as a result of the increase in oxygen requirements. The hyperperfusion phase in CBF was significantly reduced during hypoxia and ischemia showing a further decline in oxygen supply during CSD. CSD wave duration increased during the pathological conditions, showing a disturbance in energy production.Extracellular K(+) levels during CSD, increased to identical levels during normoxia and during the three pathological groups, indicating correspondingly increase in oxygen demand. 5. The special design of the MPA enabled identifying differences in the simultaneous responses of the measured parameters, which may indicate changes in the interrelation between oxygen demand, oxygen supply and oxygen balance during CSD propagation, under the conditions tested. 6. In conclusion, brain oxygenation was found to be a critical factor in the responses of the brain to CSD.

No MeSH data available.


Related in: MedlinePlus

Analog tracings presenting the effect of CSD initiation during normoxia (A) and hypoxia (B). R – reflectance, NADH – mitochondrialNADH redox state; CBF– cerebral blood flow; K+e – corrected extracellular potassium concentration; DC – DC steady potential.The arrows indicate the moment of KCl solution application for induction of CSD wave. Dotted lines in 2A and 2B mark the simultaneousminimum and maximum responses in CBF and NADH during CSD.
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Figure 2: Analog tracings presenting the effect of CSD initiation during normoxia (A) and hypoxia (B). R – reflectance, NADH – mitochondrialNADH redox state; CBF– cerebral blood flow; K+e – corrected extracellular potassium concentration; DC – DC steady potential.The arrows indicate the moment of KCl solution application for induction of CSD wave. Dotted lines in 2A and 2B mark the simultaneousminimum and maximum responses in CBF and NADH during CSD.

Mentions: Fig. (2) is an analog tracing that illustrates the effect of CSD on the brain cortex during normoxia (A) and hypoxia (B) of the same animal. CSD during normoxia (A) caused a biphasic response in reflectance, an increase that was followed by a decrease. Mitochondrial NADH decreased showing an oxidation cycle, CBF and [K+]e increased and DC potential decreased. During hypoxia (B), the increase in reflectance augmented and the decrease phase reduced. NADH and CBF under hypoxic conditions changed their responses to CSD: in NADH an initial reduction cycle that was followed by a small oxidation one; CBF declined parallel to the increase in NADH and later on, a small increase was seem, which was accompanied by the small oxidation cycle in NADH. CSD during control conditions showed that the maximum (peak) in [K+]e occurred parallel to the minimum (peak) in NADH (maximum oxidation) whereas the CBF increase, started afterwards reaching the maximum level about 45 seconds later. In contradiction, the maximum (peak) in [K+]e occurred parallel to the reduction cycle in NADH and the decrease in CBF (Fig. 2B dotted lines). In addition, CSD wave duration prolonged during hypoxia as compared to normoxia.


Responses to Cortical Spreading Depression under Oxygen Deficiency.

Sonn J, Mayevsky A - Open Neurol J (2012)

Analog tracings presenting the effect of CSD initiation during normoxia (A) and hypoxia (B). R – reflectance, NADH – mitochondrialNADH redox state; CBF– cerebral blood flow; K+e – corrected extracellular potassium concentration; DC – DC steady potential.The arrows indicate the moment of KCl solution application for induction of CSD wave. Dotted lines in 2A and 2B mark the simultaneousminimum and maximum responses in CBF and NADH during CSD.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3367297&req=5

Figure 2: Analog tracings presenting the effect of CSD initiation during normoxia (A) and hypoxia (B). R – reflectance, NADH – mitochondrialNADH redox state; CBF– cerebral blood flow; K+e – corrected extracellular potassium concentration; DC – DC steady potential.The arrows indicate the moment of KCl solution application for induction of CSD wave. Dotted lines in 2A and 2B mark the simultaneousminimum and maximum responses in CBF and NADH during CSD.
Mentions: Fig. (2) is an analog tracing that illustrates the effect of CSD on the brain cortex during normoxia (A) and hypoxia (B) of the same animal. CSD during normoxia (A) caused a biphasic response in reflectance, an increase that was followed by a decrease. Mitochondrial NADH decreased showing an oxidation cycle, CBF and [K+]e increased and DC potential decreased. During hypoxia (B), the increase in reflectance augmented and the decrease phase reduced. NADH and CBF under hypoxic conditions changed their responses to CSD: in NADH an initial reduction cycle that was followed by a small oxidation one; CBF declined parallel to the increase in NADH and later on, a small increase was seem, which was accompanied by the small oxidation cycle in NADH. CSD during control conditions showed that the maximum (peak) in [K+]e occurred parallel to the minimum (peak) in NADH (maximum oxidation) whereas the CBF increase, started afterwards reaching the maximum level about 45 seconds later. In contradiction, the maximum (peak) in [K+]e occurred parallel to the reduction cycle in NADH and the decrease in CBF (Fig. 2B dotted lines). In addition, CSD wave duration prolonged during hypoxia as compared to normoxia.

Bottom Line: CSD under the 3 pathological conditions caused an initial increase in NADH and a further decrease in CBF during the first phase of CSD, indicating an imbalance between oxygen supply and demand as a result of the increase in oxygen requirements.The special design of the MPA enabled identifying differences in the simultaneous responses of the measured parameters, which may indicate changes in the interrelation between oxygen demand, oxygen supply and oxygen balance during CSD propagation, under the conditions tested. 6.In conclusion, brain oxygenation was found to be a critical factor in the responses of the brain to CSD.

View Article: PubMed Central - PubMed

Affiliation: The Mina & Everard Goodman, Faculty of Life Sciences and Leslie and Susan Gonda Multidisciplinary Brain Research Center, Bar-Ilan University RAMAT-GAN 52900, Israel.

ABSTRACT

Objectives: The effect of cortical spreading depression (CSD) on extracellular K(+) concentrations ([K(+)](e)), cerebral blood flow (CBF), mitochondrial NADH redox state and direct current (DC) potential was studied during normoxia and three pathological conditions: hypoxia, after NOS inhibition by L-NAME and partial ischemia.

Methods: A SPECIAL DEVICE (MPA) WAS USED FOR MONITORING CSD WAVE PROPAGATION, CONTAINING: mitochondrial NADH redox state and reflected light, by a fluorometry technique; DC potential by Ag/AgCl electrodes; CBF by laser Doppler flowmetry; and [K(+)](e) by a mini-electrode.

Results and discussion: CSD under the 3 pathological conditions caused an initial increase in NADH and a further decrease in CBF during the first phase of CSD, indicating an imbalance between oxygen supply and demand as a result of the increase in oxygen requirements. The hyperperfusion phase in CBF was significantly reduced during hypoxia and ischemia showing a further decline in oxygen supply during CSD. CSD wave duration increased during the pathological conditions, showing a disturbance in energy production.Extracellular K(+) levels during CSD, increased to identical levels during normoxia and during the three pathological groups, indicating correspondingly increase in oxygen demand. 5. The special design of the MPA enabled identifying differences in the simultaneous responses of the measured parameters, which may indicate changes in the interrelation between oxygen demand, oxygen supply and oxygen balance during CSD propagation, under the conditions tested. 6. In conclusion, brain oxygenation was found to be a critical factor in the responses of the brain to CSD.

No MeSH data available.


Related in: MedlinePlus