Effect of hyperbaric oxygenation on the Na+, K(+)-ATPase and membrane fluidity of cerebrocortical membranes after experimental subarachnoid hemorrhage.
It is reported that CNS hemorrhage causes membrane dysfunction and may exacerbate this damage as a result of secondary ischemia or hypoxia. Since hyperbaric oxygenation improves oxygen metabolism, it may reduce this membrane damage. The present study was conducted to reveal whether hyperbaric oxygenation influences membrane alteration after hemorrhage. Thirty minutes after subarachnoid hemorrhage induction, rats were treated with hyperbaric oxygenation 2 ATA for 1 hour. Rats were decapitated 2 hours after subarachnoid hemorrhage induction. Na+, K(+)-ATPase activity measurement and spin-label studies were performed on crude synaptosomal membranes. Subarachnoid hemorrhage decreased Na+, K(+)-ATPase activity. Spin label studies showed that hydrophobic portions of near the membrane surface became more rigid and the mobility of the membrane protein labeled sulfhydryl groups decreased after subarachnoid hemorrhage. Hyperbaric oxygenation significantly ameliorated most of the subarachnoid hemorrhage induced alterations. We conclude that hyperbaric oxygenation may be a beneficial treatment for acute subarachnoid hemorrhage.
Yufu
K
K
Department of Anesthesiology and Resuscitology, Okayama University Medical School, Japan.
Itoh
T
T
Edamatsu
R
R
Mori
A
A
Hirakawa
M
M
D000818:Animals; D002540:Cerebral Cortex / Q000187:drug effects*; D006931:Hyperbaric Oxygenation; D008297:Male; D008560:Membrane Fluidity / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D000254:Sodium-Potassium-Exchanging ATPase / Q000187:drug effects*; D013345:Subarachnoid Hemorrhage / Q000188:drug therapy* / Q000201:enzymology; D013570:Synaptic Membranes / Q000187:drug effects
D000254:Sodium-Potassium-Exchanging ATPase