Alkalinization during re-oxygenation prevents functional damage by hyperglycaemic hypoxia.
Hyperglycaemia impairs recovery from transient cerebral ischaemia: the importance of tissue acidification for this phenomenon has not been clarified in detail. We investigated this issue in a less complex in vitro preparation of isolated rat dorsal spinal roots exposed for 30 min to hyperglycaemic hypoxia. Peak height of compound action potentials recovered minimally in 5 mM bicarbonate. However, recovery was greatly improved by addition of the weak base trimethylamine during re-oxygenation. Addition of the weak acid propionate had no such effect. Cytoplasmic alkalinization improved recovery in a brief time window only: application of trimethylamine after 15 min of re-oxygenation was without beneficial effect. These data emphasize the importance of cytoplasmic acidification for neurophysiological recovery from hyperglycaemic hypoxia during the initial period of re-oxygenation.
Euchner-Wamser
I
I
Department of Physiology, University of Munich, Germany.
Grafe
P
P
Sennefelder
E
E
Schneider
U
U
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D002545:Brain Ischemia / Q000473:pathology / Q000503:physiopathology; D003593:Cytoplasm / Q000378:metabolism; D004594:Electrophysiology; D006863:Hydrogen-Ion Concentration; D006943:Hyperglycemia / Q000473:pathology* / Q000503:physiopathology; D000860:Hypoxia / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D008744:Methylamines / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000473:pathology* / Q000503:physiopathology
D008744:Methylamines; C023336:trimethylamine