| Abstract No.: | B-C2118 |
| Country: | Canada |
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| Title: | EFFECTS OF CALORIC RESTRICTION FOLLOWING GLOBAL ISCHEMIA ON LONG-TERM FUNCTIONAL OUTCOME |
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| Authors/Affiliations: | 1 Barbara Heather*; 1 Phyllis Paterson;
1 College of Pharmacy and Nutrition, University of Saskatchewan, Saskatoon, SK, Canada
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| Content: | Introduction: Stroke, a reduction in blood flow to the brain, is a major cause of death and chronic disability in North America, for which there is still limited treatment. A previous study suggested that pre-ischemic caloric restriction (CR) protects against brain damage in focal ischemia, but it was not clear if the damage was permanently decreased or only delayed. The hypothesis of this study was that post-ischemic CR, which can reduce oxidative stress and inflammation, would also cause a decrease in brain damage that would be permanent.
Objectives: The objectives were to assess the long-term (60d) effects of caloric restriction (CR) on functional and histological outcome in a gerbil model of global ischemia.
Materials and Methods: Male Mongolian gerbils (12-13 wk) underwent 5-minute bilateral common carotid artery occlusion surgery or sham surgery. Tympanic temperature was monitored and maintained during the ischemic period at 36.5 ± 0.2°C. Persistent hyperactivity was monitored for 20 h post-surgery using infrared beam interruptions as a measure of consistency of ischemic damage. Animals were then randomized to a modified AIN 93-M control (CON) diet or a 30% CR diet, reformulated to ensure the same intake of essential nutrients as the CON group. Thus, experimental groups consisted of control diet-sham surgery (CON-S), control diet-ischemia (CON-I), CR-sham surgery (CR-S) and CR-ischemia (CR-I). To test functional outcome, the gerbils were tested in the open field test on days 3, 7, 10, 30 and 60 post-ischemia (n=14-18 animals/group). Brain damage was evaluated by the ability to habituate in the open field, assessed by the distance travelled over 10 minutes. Animals were perfused at 60 d post-ischemia, and brains will be sectioned and stained with hemotoxylin and eosin for assessing the number of viable hippocampal CA1 neurons.
Results: By 60d, CR resulted in a mean (± SEM) weight loss of 26 ± 2% and 25 ± 2% in the CR-I and CR-S groups, respectively. Preliminary ANOVA indicates that total distance in the open field was greater in the ischemic animals than in sham animals on all test days (p<0.001), but this was not influenced by CR (P>0.05).
Conclusion: These findings suggest that CR administered after the insult cannot offer protection against the long-term functional deficits induced by global ischemia. The extent to which these findings correlate with hippocampal CA1 cell counts will be addressed. (Funded by the Heart and Stroke Foundation of Saskatchewan) |
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