Cardiovascular and Metabolic Disease Center
Mitochondrial Research Affinity Collaboration-Laboratories & Engineering

Home > 0

Mitochondrial Damage Impairs Oxygen Metabolism After Intracerebral Hemorrhage

  • 작성자한진
  • 작성일2007-01-11 01:11:14
  • 조회수2138
  • 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.
Total404 [ page8/27 ]
No. 제목 작성자 작성일 조회수
299 미토콘드리아 DNA를 방출하여 세균을 잡는 호산구 2008.08.19 한진 2008.08.19 2,221
298 한진교수님, 신문에 나셨어요! 2008.08.08 홍다혜 2008.08.08 2,154
297 롯데경기 다시보기 2008.07.12 최성우 2008.07.12 2,677
296 뚱뚱한 사람 ‘당뇨·심장병’ 잘 생기는 이유 찾았다 2008.07.07 한진 2008.07.07 2,232
295 Mitochondrial dysfunction and redox signaling in atrial tachyarrhythmia 2008.06.08 한진 2008.06.08 4,004
294 근위축증-세포사멸 -미토콘드리아 -네이쳐 2008.04.28 김형규 2008.04.28 4,441
293 PPAR and diabetics (PPAR 리간드로 당뇨치료) 2008.04.28 김형규 2008.04.28 3,808
292 알츠하이머 억제 효소, 다른 치매에는 악영향 (2008-04-24) 2008.04.28 김형규 2008.04.28 3,147
291 암세포 조절 유전자 -glut 3 2008.04.25 김형규 2008.04.25 3,203
290 Weekly research highlight in NATURE 2008.04.11 김형규 2008.04.11 2,872
289 "아연"이 뇌신경세포 사멸시킨다. 2008.04.11 김형규 2008.04.11 2,954
288 2008 KHUPO congress 소개 2008.04.10 김형규 2008.04.10 2,682
287 International Physiome Symposium 2008 2008.03.28 한진 2008.03.28 2,524
286 '레스베라트롤(resveratrol)이 미토콘드리아 기능을 억제하여 암세포를 죽인다. 2008.03.26 한진 2008.03.26 3,615
285 비만치료의 새 표적: 미토콘드리아 언커플링 (2008-03-16) 2008.03.19 한진 2008.03.19 2,890
처음이전 1 2 3 4 5 6 7 8 9 10 다음 마지막