Brain acidosis induced by hypercarbic ventilation attenuates focal ischemic injury.
Intracellular calcium toxicity appears to play a major role in cell death during cerebral ischemia. Such calcium enters the cell mainly through the N-methyl-D-aspartate subclass of the postsynaptic glutamate receptor. Increased extracellular hydrogen ion concentration has been shown recently to reduce N-methyl-D-aspartate-activated divalent cation currents. Therefore, we studied the effect of induced brain acidosis, via hypercarbic ventilation, as a potential therapeutic modality in focal cerebral ischemia. Brain acidosis reduced infarct volume in a biphasic manner, with maximal protection at approximately brain pH 6.8. The effect was lost at pH 6.5, presumably due to the effect of acidosis on glial glutamate uptake.
Simon
R P
RP
University of California, San Francisco.
Niro
M
M
Gwinn
R
R
D000142:Acidosis, Respiratory / Q000097:blood / Q000139:chemically induced* / Q000503:physiopathology; D000818:Animals; D001927:Brain Diseases / Q000097:blood / Q000139:chemically induced* / Q000378:metabolism; D002245:Carbon Dioxide / Q000008:administration & dosage / Q000097:blood / Q000627:therapeutic use*; D006863:Hydrogen-Ion Concentration; D002546:Ischemic Attack, Transient / Q000097:blood / Q000378:metabolism / Q000628:therapy*; D008297:Male; D010313:Partial Pressure; D051381:Rats; D017207:Rats, Sprague-Dawley
D002245:Carbon Dioxide