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 [ page9/27 ]
No. 제목 작성자 작성일 조회수
284 완전 축하 합니다 박원선 선생 둘째 아들 탄생!! 2008.02.13 김형규 2008.02.13 2,475
283 한번더 축하 드립니다 고재홍 선생님!!! 2008.01.31 강성현 2008.01.31 2,419
282 "2008년 한국생화학분자생물학회 정기 학술대회 및 대한생화학분자생물학회 통합심포지엄" 2008.01.31 한진 2008.01.31 2,998
281 연세의대 2008.01.31 한진 2008.01.31 2,431
280 칼자이스 유저 스토리 2008.01.25 한진 2008.01.25 2,267
279 아시아 미토콘드리아 의학 연구회 2008.01.14 박원선 2008.01.14 2,654
278 Coming soon, an anti-ageing injection 2007.08.19 한진 2007.08.19 2,534
277 Thanks and Good-bye from Khoa. 2007.06.28 트란민콰 2007.06.28 2,622
276 Flavored Oxygen Rocks World of Energy Drinks and Supplements 첨부파일 2007.06.25 한진 2007.06.25 3,097
275 Mitochondrial Oxidative Stress Causes Hyperphosphorylation of Tau 첨부파일 2007.06.25 한진 2007.06.25 3,083
274 Researchers identify protein pathway involved in Parkinson disease development 첨부파일 2007.06.25 한진 2007.06.25 2,528
273 I introduced our lab to people in Auckland. 첨부파일 2007.06.13 김나리 2007.06.13 2,303
272 New technique may be used with confocal microscope 첨부파일 2007.05.31 Dang Van Cuong 2007.05.31 2,050
271 New Confocal microscope in Kimhae 첨부파일 2007.05.31 Dang Van Cuong 2007.05.31 2,263
270 Congratulation Mr Kim 2007.05.25 박원선 2007.05.25 2,217
처음이전 1 2 3 4 5 6 7 8 9 10 다음 마지막