title: Sustained damage to energy metabolism of brain regions after microsphere embolism in rats.
abstract: OBJECTIVE
  Information on sustained damage to cerebral function and metabolism after cerebral ischemia is useful for prophylaxis and therapeutics of cerebral infarction. The purpose of the present study was to induce sustained damage to brain regions after cerebral ischemia in experimental animals. For this purpose, we examined animal behavior and cerebral energy metabolism following microsphere embolism in rats.
  
  
  METHODS
  We injected 900 microspheres (48 microns in diameter) into the right internal carotid artery of 110 rats and determined the time course of changes in the rats' behavior and the energy metabolism of the cortex, striatum, and hippocampus of both hemispheres. We injected the same volume of vehicle, without microspheres, into 28 sham-operated rats; there were 14 nonoperated control rats.
  
  
  RESULTS
  Peak increase in lactate content and decrease in adenosine triphosphate and creatine phosphate of these brain regions of the right hemisphere were seen on the first day after microsphere embolism, whereas peak increases in glucose and glycogen contents of these regions were observed on the third day. Most of the metabolic alterations in all these regions continued for up to 28 days after operation, although they recovered toward control levels with time after the operation. The extent and trend of metabolite changes of the right hemisphere after microsphere embolism were similar in the three brain regions. In the left hemisphere, similar metabolic changes were observed, but to a lesser degree. The time course of changes in behavioral scores following microsphere embolism revealed marked stroke-like symptoms on the first day and relatively rapid disappearance of the symptoms with time after embolism.
  
  
  CONCLUSIONS
  Microsphere embolism is capable of inducing widespread, sustained damage to energy metabolism of brain regions.
authors.affiliation: Department of Pharmacology, Tokyo College of Pharmacy, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Takeo
authors.forename: T
authors.initials: T
authors.lastname: Taguchi
authors.forename: K
authors.initials: K
authors.lastname: Tanonaka
authors.forename: K
authors.initials: K
authors.lastname: Miyake
authors.forename: T
authors.initials: T
authors.lastname: Horiguchi
authors.forename: N
authors.initials: N
authors.lastname: Takagi
authors.forename: K
authors.initials: K
authors.lastname: Fujimori
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002540:Cerebral Cortex / Q000378:metabolism*; D003342:Corpus Striatum / Q000378:metabolism*; D004734:Energy Metabolism; D005947:Glucose / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism*; D002542:Intracranial Embolism and Thrombosis / Q000378:metabolism*; D007773:Lactates / Q000378:metabolism; D019344:Lactic Acid; D008297:Male; D008863:Microspheres; D010725:Phosphocreatine / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains
chemical_list: D007773:Lactates; D010725:Phosphocreatine; D019344:Lactic Acid; D000255:Adenosine Triphosphate; D005947:Glucose