Primary spinal cord injury (SCI) results from direct mechanical damage to the spinal cord. The resulting pathochemical and pathophysiological events, including oxidative stress and inflammation, lead to secondary injury. The ability to decrease secondary injury may lead to improved recovery. Increasing glutathione production after SCI leads to decreased secondary injury. Glutamine is an important precursor to glutathione following trauma. Skeletal muscle phenotype is strongly influenced by neuromuscular activity. SCI causes myosin heavy chain (MyHC) profiles to shift towards faster isoforms in slow muscles and slower isoforms in fast muscles. The hypothesis was that glutamine, as a precursor of glutathione, administration to SCI rats would lead to better functional recovery and a more preserved MyHC phenotype in locomotory muscles. <p> Rats were assigned to one of four groups; healthy, laminectomy only, untreated SCI, and SCI treated with an intraperitoneal injection of 1mmol/kg glutamine every 12 hours for one week after injury. SCIs were performed at T6 with a modified aneurism clip. Functional recovery was measured weekly using the Basso-Beattie-Bresnahan scale and the angle board method. Six weeks later, all rats were killed, and their extensor digitorum longus and soleus muscles excised and weighed. MyHC composition of the muscles was determined using SDS-PAGE.<p>The hypothesis that glutamine treatment following SCI would lead to better functional recovery and a more preserved MyHC profile was validated. Glutamine treated rats received significantly higher BBB scores (p<0.01) and angle board scores (p<0.001) than untreated SCI rats. Glutamine treatment also reduces muscle atrophy in the soleus muscle, but not the extensor digitorum longus (EDL). In untreated rats the soleus muscle accounted for significantly (p<0.001) less of the percentage of total body weight than the soleus muscle from glutamine treated rats. Finally, SCI rats with preserved functional abilities displayed a significantly better preserved MyHC profile compared to untreated SCI rats. In the soleus healthy rats contain 94% type 1 myosin, treated rats maintained 68% which was significantly (p<0.001) greater than 28% maintained by untreated rats. In the EDL healthy rats contain 55% type 2b myosin, treated rats maintained 32% which was greater than 26% type 2b myosin maintained by untreated rats.
| Identifer | oai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:SSU.etd-04192005-153007 |
| Date | 20 April 2005 |
| Creators | Golding, Jamie Danielle |
| Contributors | Rosser, Benjamin W. C., Krone, Patrick H., Doucette, J. Ronald, West, Nigel |
| Publisher | University of Saskatchewan |
| Source Sets | Library and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada |
| Language | English |
| Detected Language | English |
| Type | text |
| Format | application/pdf |
| Source | http://library.usask.ca/theses/available/etd-04192005-153007/ |
| Rights | unrestricted, I hereby certify that, if appropriate, I have obtained and attached hereto a written permission statement from the owner(s) of each third party copyrighted matter to be included in my thesis, dissertation, or project report, allowing distribution as specified below. I certify that the version I submitted is the same as that approved by my advisory committee. I hereby grant to University of Saskatchewan or its agents the non-exclusive license to archive and make accessible, under the conditions specified below, my thesis, dissertation, or project report in whole or in part in all forms of media, now or hereafter known. I retain all other ownership rights to the copyright of the thesis, dissertation or project report. I also retain the right to use in future works (such as articles or books) all or part of this thesis, dissertation, or project report. |
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