Effects of anesthesia on the responses to cortical spreading depression in the rat brain in vivo.
OBJECTIVE
The aim of this study was to evaluate the effect of cortical spreading depression (CSD) on the metabolic, hemodynamic, electrical and ionic properties during anesthesia as compared with the awake state.


METHODS
The mitochondrial NADH redox state, reflected light, direct current (DC) potential, electrocorticography (ECoG), cerebral blood flow (CBF) and volume (CBV), and extracellular K(+) concentrations ([K(+)](e)), were measured continuously and simultaneously in real time using two unique monitoring systems that evaluate brain function. Three consecutive CSD waves were initiated using a KCl solution in both awake and anesthetized rats.


CONCLUSIONS
CSD caused typical amplitude changes: biphasic waves in reflectance, oxidation cycles in NADH, an increase in CBF, CBV and in [K(+)](e), a negative shift in DC potential and depression in ECoG. Anesthesia by equithesin decreased significantly the baseline levels of CBF and [K(+)](e), showing a reduction in oxygen supply and demand. After anesthesia, CSD significantly decreased [K(+)](e) and NADH oxidation cycles, indicating a reduction in oxygen demand and in oxygen balance, respectively. Furthermore, anesthesia reduced CSD wave frequencies by slowing the recovery period, showing a decline in energy production during brain activation, or by changing electrophysiological properties of the tissue. No changes were found in the propagation rate and in the initiation period of CSD, which may indicate that equithesin does not block CSD initiation. In addition, we found that the whole cerebral cortex reacts homogenously to CSD and that equithesin may reduce oxygen demand and energy production, which may have a protective effect on the brain exposed to pathophysiological conditions.
Faculty of Life Sciences, Bar-Ilan University, Ramat-Gan 52900, Israel. sonnju@mail.biu.ac.il
Judith
J
Sonn
Avraham
A
Mayevsky
D000777:Anesthetics / Q000494:pharmacology*; D000818:Animals; D002540:Cerebral Cortex / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology; D002697:Chloral Hydrate / Q000494:pharmacology; D013181:Cortical Spreading Depression / Q000187:drug effects* / Q000502:physiology; D004195:Disease Models, Animal; D004734:Energy Metabolism / Q000187:drug effects / Q000502:physiology; D045604:Extracellular Fluid / Q000187:drug effects / Q000378:metabolism; D008278:Magnesium Sulfate / Q000494:pharmacology; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D008928:Mitochondria / Q000378:metabolism; D009243:NAD / Q000378:metabolism; D009434:Neural Pathways / Q000187:drug effects* / Q000503:physiopathology; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism; D010084:Oxidation-Reduction / Q000187:drug effects; D010101:Oxygen Consumption / Q000187:drug effects / Q000502:physiology; D010424:Pentobarbital / Q000494:pharmacology; D010775:Photic Stimulation; D011188:Potassium / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D009435:Synaptic Transmission / Q000187:drug effects* / Q000502:physiology; D014851:Wakefulness / Q000187:drug effects / Q000502:physiology
D000777:Anesthetics; D009243:NAD; C034864:chloropent; D002697:Chloral Hydrate; D008278:Magnesium Sulfate; D010424:Pentobarbital; D011188:Potassium