Journal
MICROVASCULAR RESEARCH
Volume 81, Issue 1, Pages 73-80Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.mvr.2010.11.003
Keywords
Traumatic brain injury; Cerebral blood flow; Revascularization; EETs; Soluble epoxide hydrolase; Optical imaging
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Funding
- National Heart, Lung, and Blood Institute [R01 HL093140]
- National Institute of Biomedical Imaging and Bioengineering [R01 EB009682]
- National Institute of Deafness and other Communication Disorders [R01 DC010201]
- American Heart Association [0855733G]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL093140] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF BIOMEDICAL IMAGING AND BIOENGINEERING [R01EB009682] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS070837, R01NS044313, P30NS061800] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS [R01DC010201] Funding Source: NIH RePORTER
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Revascularization following brain trauma is crucial to the repair process. We used optical micro-angiography (OMAG) to study endogenous revascularization in living mice following brain injury. OMAG is a volumetric optical imaging method capable of in vivo mapping of localized blood perfusion within the scanned tissue beds down to capillary level imaging resolution. We demonstrated that OMAG can differentiate revascularization progression between traumatized mice with and without soluble epoxide hydrolase (sEH) gene deletion. The time course of revascularization was determined from serial imaging of the traumatic region in the same mice over a one-month period of rehabilitation. Restoration of blood volume at the lesion site was more pronounced in sEH knockout mice than in wild-type mice as determined by OMAG. These OMAG measurements were confirmed by histology and showed that the sEH knockout effect may be involved in enhancing revascularization. The correlation of OMAG with histology also suggests that OMAG is a useful imaging tool for real-time in vivo monitoring of post-traumatic revascularization and for evaluating agents that inhibit or promote endogenous revascularization during the recovery process in small rodents. Published by Elsevier Inc.
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