期刊
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
卷 32, 期 8, 页码 1525-1534出版社
SAGE PUBLICATIONS INC
DOI: 10.1038/jcbfm.2012.38
关键词
cardiac arrest; hypothermia; neuroprotection; stroke; synchrotron; temperature
资金
- Canadian Institutes of Health Research (CIHR)
- CIHR/Heart and Stroke Foundation of Canada [CIF 99472]
- focus on stroke doctoral scholarship
- McCormick Fellowship
- DOE Office of Biological and Environmental Research
- National Institutes of Health, National Center for Research Resources, Biomedical Technology Program [P41RR001209]
Hypothermia improves clinical outcome after cardiac arrest in adults. Animal data show that a day or more of cooling optimally reduces edema and tissue injury after cerebral ischemia, especially after longer intervention delays. Lengthy treatments, however, may inhibit repair processes (e. g., synaptogenesis). Thus, we evaluated whether unilateral brain hypothermia (similar to 33 degrees C) affects neuroplasticity in the rat 2-vessel occlusion model. In the first experiment, we cooled starting 1 hour after ischemia for 2, 4, or 7 days. Another group was cooled for 2 days starting 48 hours after ischemia. One group remained normothermic throughout. All hypothermia treatments started 1 hour after ischemia equally reduced hippocampal CA1 injury in the cooled hemisphere compared with the normothermic side and the normothermic group. Cooling only on days 3 and 4 was not beneficial. Importantly, no treatment influenced neurogenesis (Ki67/Doublecortin (DCX) staining), synapse formation (synaptophysin), or brain-derived neurotropic factor (BDNF) immunohistochemistry. A second experiment confirmed that BDNF levels (ELISA) were equivalent in normothermic and 7-day cooled rats. Last, we measured zinc (Zn), which is important in plasticity, with X-ray fluorescence imaging in normothermic and 7-day cooled rats. Hypothermia did not alter the postischemic distribution of Zn within the hippocampus. In summary, cooling significantly mitigates injury without compromising neuroplasticity. Journal of Cerebral Blood Flow & Metabolism (2012) 32, 1525-1534; doi: 10.1038/jcbfm.2012.38; published online 21 March 2012
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