title: [Changes in cerebral energy and calcium metabolisms on focal cerebral ischemia].
abstract: Changes of brain tissue calcium in the focal ischemia model of Wistar rat were investigated by three different methods; atomic absorption spectrophotometer, calcium stain with alizarin red S, and new histochemical method using aequorin, a calcium ion sensitive photoprotein. Tissue pH and tissue ATP were concomitantly investigated by histochemical method. Rat brain was frozen in situ at 15, 60 or 240 minutes after left middle cerebral artery was occluded. Coronal brain sections of 16 microns thickness was made and the brain slices applied for calcium stain and histochemical studies. The residual brain block was applied for atomic absorption spectrophotometric study. Tissue calcium content of left hemisphere increased from 1.34 +/- 0.09 (mean +/- SEM) (n = 7) to 1. 54 +/- 0.16 (n = 12), 2.07 +/- 0.12 (n = 9). 1.69 +/- 0.11 (n = 10) mumol/g wet weight after 15, 60 and 240 minutes respectively. Calcium stain with alizarin red S showed that the increase of calcium was observed in the peripheral part of the ischemic lesion where ATP was left in a spotty fashion, and calcium deposits disappeared with correspondence to exhaustion of ATP. Tissue calcium ion content studied by newly histochemical method, showed heterogeneous change. At an early stage of the ischemia, the increase of tissue calcium ion was shown only in the peripheral part of the ischemic lesion, and it gradually extended to the central part. Calcium ion increased in density in an area corresponding to that of the ATP decrease. Within the area of calcium ion increase, regional differences were noted; a greater increase at the border with the intact area and in the parts where ATP was heterogeneously preserved. In the non-ischemic area close to the ischemic area, where ATP was preserved with mild acidosis, calcium ion decreased more than in the surrounding area where ATP was preserved.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Neurosurgery, Faculty of Medicine, Kyoto University, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Hashimoto
authors.forename: H
authors.initials: H
authors.lastname: Kikuchi
authors.forename: M
authors.initials: M
authors.lastname: Ishikawa
authors.forename: S
authors.initials: S
authors.lastname: Kobayashi
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000331:Aequorin; D000818:Animals; D001921:Brain / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism*; D004734:Energy Metabolism; D006651:Histocytochemistry / Q000379:methods; D006863:Hydrogen-Ion Concentration; D002546:Ischemic Attack, Transient / Q000378:metabolism*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains
chemical_list: D000331:Aequorin; D000255:Adenosine Triphosphate; D002118:Calcium