Effect of traumatic brain injury and nitrone radical scavengers on relative changes in regional cerebral blood flow and glucose uptake in rats
(2002) In Journal of Neurotrauma 19(10). p.53-1139- Abstract
Changes in regional cerebral blood flow (rCBF) and glucose metabolism are commonly associated with traumatic brain injury (TBI). Reactive oxygen species (ROS) have been implicated as key contributors to the secondary injury process after TBI. Here, pretreatment with the nitrone radical scavengers (alpha-phenyl-N-tert-butyl nitrone (PBN) or its sulfonated analogue sodium 2-sulfophenyl-N-tert-butyl nitrone (S-PBN) were used as tools to study the effects of ROS on rCBF and glucose metabolism after moderate (2.4-2.6 atm) lateral fluid percussion injury (FPI) in rats. S-PBN has a half-life in plasma of 9 min and does not penetrate the blood-brain barrier (BBB). In contrast, PBN has a half-life of 3 h and readily penetrates the BBB. Regional... (More)
Changes in regional cerebral blood flow (rCBF) and glucose metabolism are commonly associated with traumatic brain injury (TBI). Reactive oxygen species (ROS) have been implicated as key contributors to the secondary injury process after TBI. Here, pretreatment with the nitrone radical scavengers (alpha-phenyl-N-tert-butyl nitrone (PBN) or its sulfonated analogue sodium 2-sulfophenyl-N-tert-butyl nitrone (S-PBN) were used as tools to study the effects of ROS on rCBF and glucose metabolism after moderate (2.4-2.6 atm) lateral fluid percussion injury (FPI) in rats. S-PBN has a half-life in plasma of 9 min and does not penetrate the blood-brain barrier (BBB). In contrast, PBN has a half-life of 3 h and readily penetrates the BBB. Regional cerebral blood flow (rCBF) and glucose metabolism was estimated by using (99m)Tc-HMPAO and [(18)F]Fluoro-2-deoxyglucose (FDG) autoradiography, respectively, at 42 min (n = 37) and 12 h (n = 34) after the injury. Regions of interest were the parietal cortex and hippocampus bilaterally. As expected, FPI produced an early (42-min) hypoperfusion in ipsilateral cortex and an increase in glucose metabolism in both cortex and hippocampus, giving way to a state of hypoperfusion and decreased glucose metabolism at 12 h postinjury. On the contralateral side, a hypoperfusion in the cortex and hippocampus was seen at 12 h only, but no significant changes in glucose metabolism. Both S-PBN and PBN attenuated the trauma-induced changes in rCBF and glucose metabolism. Thus, the early improvement in rCBF and glucose metabolism correlates with and may partly mediate the improved functional and morphological outcome after TBI in nitrone-treated rats.
(Less)
- author
- Marklund, Niklas LU ; Sihver, Sven ; Långström, Bengt ; Bergström, Mats and Hillered, Lars
- publishing date
- 2002-10
- type
- Contribution to journal
- publication status
- published
- keywords
- Animals, Benzenesulfonates, Brain Injuries, Cerebrovascular Circulation, Cyclic N-Oxides, Fluorodeoxyglucose F18, Free Radical Scavengers, Glucose, Hippocampus, Male, Neuroprotective Agents, Nitrogen Oxides, Radiopharmaceuticals, Rats, Rats, Sprague-Dawley, Reactive Oxygen Species, Technetium Tc 99m Exametazime, Journal Article, Research Support, Non-U.S. Gov't
- in
- Journal of Neurotrauma
- volume
- 19
- issue
- 10
- pages
- 15 pages
- publisher
- Mary Ann Liebert, Inc.
- external identifiers
-
- pmid:12427324
- scopus:0036800136
- ISSN
- 0897-7151
- DOI
- 10.1089/08977150260337958
- language
- English
- LU publication?
- no
- id
- f476d972-e2ea-40d9-834f-c3cd9805e8a7
- date added to LUP
- 2016-12-08 12:16:31
- date last changed
- 2024-05-31 19:09:17
@article{f476d972-e2ea-40d9-834f-c3cd9805e8a7, abstract = {{<p>Changes in regional cerebral blood flow (rCBF) and glucose metabolism are commonly associated with traumatic brain injury (TBI). Reactive oxygen species (ROS) have been implicated as key contributors to the secondary injury process after TBI. Here, pretreatment with the nitrone radical scavengers (alpha-phenyl-N-tert-butyl nitrone (PBN) or its sulfonated analogue sodium 2-sulfophenyl-N-tert-butyl nitrone (S-PBN) were used as tools to study the effects of ROS on rCBF and glucose metabolism after moderate (2.4-2.6 atm) lateral fluid percussion injury (FPI) in rats. S-PBN has a half-life in plasma of 9 min and does not penetrate the blood-brain barrier (BBB). In contrast, PBN has a half-life of 3 h and readily penetrates the BBB. Regional cerebral blood flow (rCBF) and glucose metabolism was estimated by using (99m)Tc-HMPAO and [(18)F]Fluoro-2-deoxyglucose (FDG) autoradiography, respectively, at 42 min (n = 37) and 12 h (n = 34) after the injury. Regions of interest were the parietal cortex and hippocampus bilaterally. As expected, FPI produced an early (42-min) hypoperfusion in ipsilateral cortex and an increase in glucose metabolism in both cortex and hippocampus, giving way to a state of hypoperfusion and decreased glucose metabolism at 12 h postinjury. On the contralateral side, a hypoperfusion in the cortex and hippocampus was seen at 12 h only, but no significant changes in glucose metabolism. Both S-PBN and PBN attenuated the trauma-induced changes in rCBF and glucose metabolism. Thus, the early improvement in rCBF and glucose metabolism correlates with and may partly mediate the improved functional and morphological outcome after TBI in nitrone-treated rats.</p>}}, author = {{Marklund, Niklas and Sihver, Sven and Långström, Bengt and Bergström, Mats and Hillered, Lars}}, issn = {{0897-7151}}, keywords = {{Animals; Benzenesulfonates; Brain Injuries; Cerebrovascular Circulation; Cyclic N-Oxides; Fluorodeoxyglucose F18; Free Radical Scavengers; Glucose; Hippocampus; Male; Neuroprotective Agents; Nitrogen Oxides; Radiopharmaceuticals; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species; Technetium Tc 99m Exametazime; Journal Article; Research Support, Non-U.S. Gov't}}, language = {{eng}}, number = {{10}}, pages = {{53--1139}}, publisher = {{Mary Ann Liebert, Inc.}}, series = {{Journal of Neurotrauma}}, title = {{Effect of traumatic brain injury and nitrone radical scavengers on relative changes in regional cerebral blood flow and glucose uptake in rats}}, url = {{http://dx.doi.org/10.1089/08977150260337958}}, doi = {{10.1089/08977150260337958}}, volume = {{19}}, year = {{2002}}, }