The effect of transient ischemia on fatty acid and lipid metabolism in the gerbil brain.
Brain ischemia was produced in gerbils by contemporary occlusion of both carotid arteries. Definite changes of the energy state in brain demonstrated that carotid occlusion was effective. At short time intervals from occlusion the free fatty acid content, their distribution, and their concentration and specific activity in arachidonate were determined in brain. A noticeable increase of the arachidonate pool and that of other free fatty acids was detected at very early times from occlusion. Specific activity by arachidonate increased after 30-60 seconds from ligation. By examining arachidonate distribution and specific activity in neutral and polar lipids of brain, it is concluded that phosphatidylcholine and phosphatidylinositol represent the more important source for the release of arachidonate during ischemia. Enzymic-mediated phenomena produced free arachidonate from lipids by a mechanism yielding diglycerides further transformed into fatty acids and by lipid degradation through phospholipase A activity.
D000818:Animals; D001921:Brain / Q000378:metabolism*; D002339:Carotid Arteries; D004075:Diglycerides / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000378:metabolism*; D005849:Gerbillinae; D002546:Ischemic Attack, Transient / Q000378:metabolism*; D050356:Lipid Metabolism; D014280:Triglycerides / Q000378:metabolism
D004075:Diglycerides; D005230:Fatty Acids, Nonesterified; D014280:Triglycerides