INVESTIGATION OF MOLECULAR MECHANISM ON ISCHEMIC

1997 Fiscal Year Final Research Report Summary

• Project/Area Number: 08671576
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Cerebral neurosurgery
• Research Institution: TAZUKE-KOFUKAI MEDICAL RESEARCH INSTITUTE (1997); Kyoto University (1996)
• Principal Investigator: ISHIKAWA Masatsune TAZUKE-KOFUKAI MEDICAL RESEARCH INSTITUTE IV OF ONOCOLOGY, 医学研究所・第4研究部, 研究主幹 (20115786)
• Project Period (FY): 1996 – 1997
• Keywords: cerebral ischemia / apoptosis / spredding depression / ischemic tolerance / apoptosis / necrosis

Research Abstract

1)Effect on brain energy metabolism
Experimantal study using adult rats revealed that loading of single spreading depression (SD) cause local acidosis in the cortex stimulated directly., followed by it extension into the ipsilateral whole hemisphere. This change was recooverd 20 minutes after stimulation. ATP histochemistry showed same change as that of tissue pH change. The repetitive loading for 120 minutes caused acidosis and ATP depletion for- 45 minutes, which was recovered 60 minutes after stimulation. Thereafter, no change could induced up to six hours later.
2)Effect on apoptosis
Apotosis in the cerebral cortex induced by cerebral ischemia was suppressed by preloading of SD.In contrast, necrosis in the cerebral corrtex was not suppredded.
3)Effect on calcium homeostasis
No calcium ion change was observed histochemically on SD loading.
Thus, present study revealed that SD protected apoptotic cell death in the cerebral cortex induced by cerebral ischemia.