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 [ page5/27 ]
No. 제목 작성자 작성일 조회수
344 BPB 논문 accept소식 2009.10.06 박원선 2009.10.06 2,067
343 p53의 활성화에 따른 지방조직의 노화가 당뇨병을 유발 2009.09.02 한진 2009.09.02 2,033
342 "인삼성분, 관절염 치료에 효과" 2009.08.09 하승희 2009.08.09 1,986
341 기능이 떨어진 미토콘드리아가 노화를 억제? 2009.07.24 홍다혜 2009.07.24 3,476
340 콜라 너무 많이 마시면... 2009.05.21 홍다혜 2009.05.21 2,250
339 Exercise and Vitamins: Now, Wait A Minute. . 첨부파일 2009.05.15 한진 2009.05.15 5,478
338 인간의 두 얼굴. 상황의 힘 2009.04.27 최성우 2009.04.27 2,011
337 인제대학교 개교 30주년 기념 해외석학(Denis Noble 교수) 초청강연 첨부파일 2009.04.26 이소라 2009.04.26 2,704
336 미토콘드리아의 신비를 밝히다 첨부파일 2009.04.10 홍다혜 2009.04.10 2,299
335 심장 세포, 매년 1% 재생 2009.04.06 홍다혜 2009.04.06 1,854
334 급성 심장사와 연관된 10개의 유전자를 확인 2009.03.28 홍다혜 2009.03.28 1,837
333 제 2형 당뇨병을 부르는 낮잠 2009.03.18 홍다혜 2009.03.18 2,014
332 부산대 수지상세포 국가지정연구실 Int J Immunopathol Pharmacol논문 개제 2009.03.11 박원선 2009.03.11 2,549
331 심장 비대와 연관된 새로운 세포 경로 규명 첨부파일 2009.03.03 홍다혜 2009.03.03 3,704
330 줄기세포연구과정에서 발견한 제2형 당뇨병의 기작 2009.02.26 한진 2009.02.26 2,443
처음이전 1 2 3 4 5 6 7 8 9 10 다음 마지막