Hemodynamic and histological effects of traumatic brain injury in eNOS-deficient mice.
(2009) In Journal of Neurotrauma 26(11). p.1953-1962- Abstract
- 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,... (More)
- 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. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1511716
- author
- Lundblad, Cornelia LU ; Grände, Per-Olof LU and Bentzer, Peter LU
- organization
- publishing date
- 2009
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Journal of Neurotrauma
- volume
- 26
- issue
- 11
- pages
- 1953 - 1962
- publisher
- Mary Ann Liebert, Inc.
- external identifiers
-
- wos:000272049600011
- pmid:19929218
- scopus:75449085574
- ISSN
- 1557-9042
- DOI
- 10.1089/neu.2009.0955
- language
- English
- LU publication?
- yes
- id
- 10507b6e-2d94-4317-8ae9-20ad9fa0fa74 (old id 1511716)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/19929218?dopt=Abstract
- date added to LUP
- 2016-04-04 09:23:33
- date last changed
- 2022-01-29 17:38:33
@article{10507b6e-2d94-4317-8ae9-20ad9fa0fa74,
abstract = {{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.}},
author = {{Lundblad, Cornelia and Grände, Per-Olof and Bentzer, Peter}},
issn = {{1557-9042}},
language = {{eng}},
number = {{11}},
pages = {{1953--1962}},
publisher = {{Mary Ann Liebert, Inc.}},
series = {{Journal of Neurotrauma}},
title = {{Hemodynamic and histological effects of traumatic brain injury in eNOS-deficient mice.}},
url = {{http://dx.doi.org/10.1089/neu.2009.0955}},
doi = {{10.1089/neu.2009.0955}},
volume = {{26}},
year = {{2009}},
}