| Hemodynamic and histological effects of traumatic brain injury in eNOS-deficient mice. | |
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MedLine Citation:
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PMID: 19929218 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Microvascular dysfunction in the brain, characterized by vasoconstriction, vascular occlusion, and disruption of the blood brain barrier, may adversely affect outcome following traumatic brain injury (TBI). Because of its vasodilating and antiaggregative properties, nitric oxide (NO) produced by nitric oxide synthase in the endothelium (eNOS) is a key regulator of vascular homeostasis. The objective of the present study was to evaluate the role of eNOS in vascular disturbances and histological outcome in the brain following TBI. Cortical blood flow ([(14)C]-iodoantipyrine technique), number of perfused capillaries (FITC-dextran technique), brain water content (wet vs. dry weight), and the transfer constant (K(i)) for [(51)Cr]-EDTA, reflecting permeability, were analyzed 3 h and 24 h after a controlled cortical impact injury (CCI) in eNOS-deficient (eNOS-KO) and wild-type (WT) mice. Cortical contusion volume and cell count in the hippocampus were evaluated 3 weeks after injury. Blood flow in the injured cortex decreased in both groups following trauma. There were no significant differences between the groups at 3 h, but blood flow was lower in eNOS-KO mice than in WT mice 24 h after trauma. Brain water content was higher in the WT mice than in eNOS-KO mice at 24 h. Number of perfused capillaries, K(i), and histological outcome were similar in both groups. We conclude that eNOS is important for maintenance of cerebral blood flow after trauma and that eNOS promotes edema formation by mechanisms other than increased permeability. The vascular effects of eNOS do not, however, influence histological outcome. |
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Authors:
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Cornelia Lundblad; Per-Olof Gr??nde; Peter Bentzer |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of neurotrauma Volume: 26 ISSN: 1557-9042 ISO Abbreviation: J. Neurotrauma Publication Date: 2009 Nov |
Date Detail:
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Created Date: 2009-11-25 Completed Date: 2010-02-02 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8811626 Medline TA: J Neurotrauma Country: United States |
Other Details:
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Languages: eng Pagination: 1953-62 Citation Subset: IM |
Affiliation:
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Department of Anesthesiology and Intensive Care, University of Lund and Lund University Hospital, Sweden. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Brain Edema / metabolism Brain Injuries / metabolism, pathology*, physiopathology* Cerebral Cortex / blood supply, pathology Cerebrovascular Circulation / physiology* Hemodynamics / physiology* Mice Mice, Knockout Nitric Oxide Synthase Type III / metabolism* |
| Chemical | |
Reg. No./Substance:
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EC 1.14.13.39/Nitric Oxide Synthase Type III |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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