engleski

Dynamics of individual brain free acids under hypoxic conditions in rats

Although considerable efforts have been directed toward characterizing the pathophysiological and neurochemical aberrations produced by hypoxia, the precise mechanisms of the ensuing brain dysfunction remain unclear. There are, however, good evidences that a variety of central nervous system changes are associated with hypoxia, including alterations of electrolyte homeostasis, depletion of energy stores, acidosis, lactacidosis, changes of blood-brain barrier permeability, decrease in membrane phospholipid content., increase of intracellular free fatty acid (FFA) pool, and the formation of free radicals. The FFAs, especially free arachidonic acid (FAA), are assumed to have detrimental effects on mitochondrial and plasma membrane functions, leading into a membrane dissolution, a production of vasoconstrictive prostaglandines and tromboxanes and an increase in neurotransmitter release. All these factors may contribute to vasoconstriction, impairment of posthypoxic reperfusion, brain vessel damage and cerebral edema, ultimately leading into the neuronal death. The present study was undertaken to examine dynamics of brain free palmitic, stearic, oleic and FAA during various time intervals after hypoxic brain injury. The study was carried out on Hannover-Wistar rats, weighing 250 g. The animals were subjected to 3.5 V% hypoxia, until loosing of righting reflex. Immediately or 5 or 15 or 60 minutes after hypoxia animals were decapitated, brains were removed quickly and frozen in the liquid nitrogen. Lipids were extracted from frozen brains and fractionated by TLC. Fatty acid methyl esters were prepared by methanolysis and quantified by GLC using internal standard method. Our results clearly demonstrated that cerebral hypoxia induced progressive increase in the brain FFA acid content. Palmitic, stearic and oleic acids show same liberation pattern, reaching statistically significant level 60 minutes after the loosing of righting reflex. Maximal level of the FAA was detected 15 minutes after cerebral hypoxia had been obtained. Sixty minutes after hypoxia procedure the level of mentioned free fatty acid decreased to the control value. It could be concluded that cerebral hypoxia induced different liberation modes of individual FFAs.

free arachidonic acid; brain; hypoxia; rat

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