Changes during ischaemia in extracellular potassium ion concentration of the brain under nitrous oxide or hexobarbital-sodium anaesthesia and moderate hypothermia.
Changes in the time lag until a steep increase in cerebral extracellular potassium ion concentration occurring during total ischaemia caused by clamping of the aorta were investigated in dogs. The results indicate that during two subsequent clamping of the aorta in the same animal the time lag between the start of ischaemia and the steep increase in potassium ion concentration (1) hardly changed during nitrous oxide anaesthesia, i.e. from 2.09 +/- 0.31 to 2.22 +/- 0.51 min; (2) as a response to the administration of hexobarbital-sodium the steep increase took place 0.50 +/- 0.37 min later, i.e. 2.89 +/- 0.74 min after the administration of the drug and then, at the second clamping, 2.39 +/- 0.71 min; (3) during a 1 degree C decrease in body temperature the steep increase took place 0.29 +/- 0.05 min later. From the values of cerebral extracellular potassium ion concentration during ischaemia the conclusion might be drawn that hypothermia serves as the principal factor in the protection of the ischaemic brain tissue; meanwhile, also hexobarbital-sodium has a significant though somewhat smaller protective effect.
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D000758:Anesthesia; D000818:Animals; D001831:Body Temperature; D001921:Brain / Q000378:metabolism; D002545:Brain Ischemia / Q000378:metabolism*; D004285:Dogs; D004569:Electroencephalography; D005110:Extracellular Space / Q000378:metabolism; D006591:Hexobarbital; D007035:Hypothermia / Q000378:metabolism*; D009609:Nitrous Oxide; D009994:Osmolar Concentration; D011188:Potassium / Q000097:blood / Q000378:metabolism*; D012890:Sleep / Q000502:physiology
D006591:Hexobarbital; D009609:Nitrous Oxide; D011188:Potassium