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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 on the measured parameters of three (A, B and C) different partial ischemic brains.Abbreviations as explained in Figs. (2 and 4).
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Figure 6: Analog tracings presenting the effect of CSD on the measured parameters of three (A, B and C) different partial ischemic brains.Abbreviations as explained in Figs. (2 and 4).

Mentions: Inductions of CSDs under ischemic conditions caused 3 kinds of variable responses (in different rats) in the measured parameters and are demonstrated in Fig. (6). Fig. (6A) shows that during CSD NADH increased, CBF decreased first, and only later, increased slightly (during the recovery phase). Extracellular K+ increased and DC potential decreased. Trace 6B shows a large increase in reflectance followed by a small decrease, an increase followed by a decrease in NADH redox state, and a clear initial deep decrease in CBF, that was followed by an increase. Trace 6C shows an increase in NADH and in CBF. In all the ischemic traces (Fig. 6) reflectance changed in a biphasic manner, an increase that was followed by a decrease and the time to recovery from CSD was prolonged (in all the measured parameters) as compared to normoxic conditions (for example Figs. 2A, 4A).


Responses to Cortical Spreading Depression under Oxygen Deficiency.

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

Analog tracings presenting the effect of CSD on the measured parameters of three (A, B and C) different partial ischemic brains.Abbreviations as explained in Figs. (2 and 4).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 6: Analog tracings presenting the effect of CSD on the measured parameters of three (A, B and C) different partial ischemic brains.Abbreviations as explained in Figs. (2 and 4).
Mentions: Inductions of CSDs under ischemic conditions caused 3 kinds of variable responses (in different rats) in the measured parameters and are demonstrated in Fig. (6). Fig. (6A) shows that during CSD NADH increased, CBF decreased first, and only later, increased slightly (during the recovery phase). Extracellular K+ increased and DC potential decreased. Trace 6B shows a large increase in reflectance followed by a small decrease, an increase followed by a decrease in NADH redox state, and a clear initial deep decrease in CBF, that was followed by an increase. Trace 6C shows an increase in NADH and in CBF. In all the ischemic traces (Fig. 6) reflectance changed in a biphasic manner, an increase that was followed by a decrease and the time to recovery from CSD was prolonged (in all the measured parameters) as compared to normoxic conditions (for example Figs. 2A, 4A).

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