Free fatty acid accumulation in the pathogenesis and therapy of ischemic-anoxic brain injury.
Energy depletion and lactate are at plateau levels within five minutes of complete ischemic-anoxia in the brain; however, irreversible brain injury has not occurred in this time. Brain free fatty acids (FFA) rise sharply during the first five minutes of ischemic-anoxia, but then continue to rise during the following hour without plateauing. Barbiturate anesthesia preischemia attenuates the FFA rise. Other agents which also attenuate the FFA increase include, among others, phenytoin and Innovar. The Ca2+ antagonists flunarizine and gallopamil also attenuated FFA rise, but were not as effective as pentobarbital during ischemia. Protective effects of Ca2+ antagonists may be more important during recirculation than during ischemia.
D000818:Animals; D002545:Brain Ischemia / Q000188:drug therapy / Q000378:metabolism*; D002936:Cinnarizine / Q000031:analogs & derivatives / Q000627:therapeutic use; D005230:Fatty Acids, Nonesterified / Q000378:metabolism*; D005444:Flunarizine; D005711:Gallopamil / Q000627:therapeutic use; D002534:Hypoxia, Brain / Q000188:drug therapy / Q000378:metabolism*; D010424:Pentobarbital / Q000627:therapeutic use; D012377:Rodentia; D012965:Sodium Chloride / Q000627:therapeutic use
D005230:Fatty Acids, Nonesterified; D005711:Gallopamil; D002936:Cinnarizine; D012965:Sodium Chloride; D010424:Pentobarbital; D005444:Flunarizine