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Barbiturate Attenuation of Brain Free Fatty Acid Liberation During Global Ischemia
Author(s) -
Shiu Gerald K.,
Nemoto Edwin M.
Publication year - 1981
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1981.tb06314.x
Subject(s) - pentobarbital , barbiturate , arachidonic acid , chemistry , stearic acid , liberation , endocrinology , medicine , ischemia , fatty acid , anesthesia , biochemistry , enzyme , organic chemistry , in vitro
To find a biochemical basis for the increased tolerance of the brain to anoxia during barbiturate anesthesia, we studied whole‐brain free fatty acids (FFA) at various times after decapitation of awake and pentobarbital‐anesthetized rats. Post‐decapitation, the brains were kept at 37°C for 1 to 60 min before freezing in liquid N 2 . Nonischemic brains were frozen in liquid N 2 , using a rapid sampling technique. Whole‐brain arachidonic, stearic, oleic, linoleic, and palmitic acids were quantitated by gas‐liquid chromatography. In unanesthetized, nonischemic brain, total FFA was 1226 ± 121 nmol/g brain ( n = 12) and was unaffected by pentobarbital anesthesia (1126 ± 86 nmol/g brain, n = 11), except for a reduction in arachidonic acid. Total FFA in unanesthetized and pentobarbital‐anesthetized rats transiently declined between 0 and 1 min of ischemia, and then rose linearly for up to 60 min, with consistently lower values in pentobarbital‐treated rats, the greatest attenuation being that of arachidonic and stearic acid liberation. Brain FFA liberation during global ischemia is the first known biochemical variable directly correlated with the duration (i.e., severity) of global ischemia. The attenuation of brain FFA liberation and especially of arachidonic and stearic acids may be the biochemical basis of barbiturate attenuation of ischemic brain injury.