Potassium ion homeostasis and mitochondrial redox status of turtle brain during and after ischemia.
To account for the remarkable capacity of turtle brain to survive without oxygen, microelectrode recordings of extracellular potassium activity (K+o) were made in intact brains of normoxic pentobarbital-anesthetized turtles during and after ischemia. Changes in redox status of brain cytochrome a,a3 were recorded simultaneously by reflection spectrophotometry. Cytochrome a,a3 became fully reduced, and K+o rose at a slow rate for approximately 60 min during complete ischemia. When K+o reached 8-12 mM, an inflection point was observed after which K+o rapidly increased to levels above 30 mM. Full recovery of baseline K+o and cytochrome a,a3 redox state occurred only if brain blood flow was restored within 60 min. These data demonstrate that maintenance of ion homeostasis in turtle brain depends on blood flow and continued delivery of systemic substrates and that viability is threatened if ischemia is prolonged beyond 60 min.
Sick
T J
TJ
Chasnoff
E P
EP
Rosenthal
M
M
D000818:Animals; D001794:Blood Pressure; D001921:Brain / Q000503:physiopathology*; D002545:Brain Ischemia / Q000503:physiopathology*; D004558:Electric Stimulation; D003576:Electron Transport Complex IV / Q000032:analysis; D004837:Epinephrine / Q000494:pharmacology; D005071:Evoked Potentials; D006706:Homeostasis; D008928:Mitochondria / Q000502:physiology*; D010084:Oxidation-Reduction; D011188:Potassium / Q000502:physiology*; D014426:Turtles / Q000502:physiology*
D003576:Electron Transport Complex IV; D011188:Potassium; D004837:Epinephrine