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Mitochondrial Damage Impairs Oxygen Metabolism After Intracerebral Hemorrhage

  • 작성자한진
  • 작성일2007-01-11 01:11:14
  • 조회수2141
  • 첨부파일첨부파일
By Will Boggs, MD NEW YORK (Reuters Health) Nov 01 - Mitochondrial damage around the hematoma, not ischemia, accounts for the reduced oxygen metabolism after intracerebral hemorrhage, according to a report in the October issue of Stroke. A primary reduction in brain metabolism follows ischemia, the authors explain, and this reduced brain metabolism is responsible for reduced cerebral blood flow and low oxygen extraction surrounding the hematoma. Dr. Jeong Sook Kim-Han and colleagues from Washington University, St. Louis, Missouri investigated whether mitochondrial function was impaired in intracerebral hemorrhage (ICH) by assessing mitochondrial respiration in perihematomal tissue removed during evacuation from 6 patients with acute spontaneous ICH compared to nonfocal tissue removed at the time of temporal lobe resection for the treatment of intractable epilepsy from 6 other patients. Tissues from ICH patients showed 40% lower oxygen consumption during state 3 respiration than control tissues, the researchers report. State 4 respiration was also reduced, the investigators say, reflecting inefficient mitochondrial energy production. State 3 and 4 respiration remained reasonable within the first 2 hours after hemorrhage, the results indicate, but mitochondria isolated after longer periods were extremely impaired. "I think the importance of this work is that it points to an entirely new concept in understanding brain injury following intracerebral hemorrhage," coinvestigator Dr. Michael Diringer told Reuters Health. "For decades it was thought that ischemia was an important cause of secondary injury in both head injury and intracerebral hemorrhage. Recent work suggests the rather than ischemia, mitochondrial function is an important issue. The distinction is very important in that therapies directed toward ischemia are unlikely to help." "We are very early in understanding this issue," Dr. Diringer said. "There are drugs used to modulate mitochondria in animals, but further work is needed to see if they would be safe and useful in humans. Another option is to give supplemental oxygen in an attempt to improve mitochondrial function." Stroke 2006;37:2457-2462,2445.
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