Artikel
Early Hypothermia attenuates neurological deficits and brain damage after experimental SAH
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Veröffentlicht: | 9. Juni 2017 |
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Gliederung
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Objective: Metabolic exhaustion in ischemic tissue is the basis for a detrimental cascade of cell damage eventually ischemic cell death. In the acute stage of subarachnoid hemorrhage (SAH), a sequence of global and focal ischemia occurs threatening brain tissue to undergo ischemic damage. This study was conducted to investigate whether early therapy with moderate hypothermia can offer neuroprotection after experimental SAH in rats.
Methods: 20 male Sprague-Dawley rats were subjected to SAH by the endovascular filament model and treated by active cooling (34° C) from 15 to 180 minutes after vessel perforation or served as controls by continuous maintainance of normothermia (37.5° C). Mean arterial blood pressure (MABP), intracranial pressure (ICP), and local CBF over both hemispheres were continuously measured. Neurological assessment was performed 24 hours later. Hippocampal damage was assessed by H.E.- and Caspase-3 staining.
Results: By a slight increase of MABP in the cooling phase and a significant reduction of ICP, hypothermia improved cerebral perfusion pressure (CPP) in the first 60 minutes after SAH. Accordingly, a trend to increased CBF was observed during this period. Thereafter, CBF was lower in hypothermic animals. The rate of injured neurons was significantly reduced in hypothermia-treated animals (4.5 ± 3 %) compared to normothermic controls (20.8 ± 4 %). The number of Caspase 3 positive neurons in the hippocampal CA1-field was reduced but did not reach the level of significance.
Conclusion: In this study, the effects of very early temporary hypothermia was investigated. The results of this series cannot finally answer whether this form of treatment permanently attenuates or only delays ischemic damage. In the latter case, slowing down metabolic exhaustion by hypothermia may still be a valuable treatment during this state of ischemic brain damage and prolong the therapeutical window for possible causal treatments of the acute perfusion deficit. Therefore, it may be useful as a first-tier therapy in suspected SAH.