Article
Acute changes of neurovascular coupling following cortical spreading depression in anesthetized rats
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Authors
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Ute Lindauer
- Experimental Neurosurgery, Department of Neurosurgery, Klinikum rechts der Isar, Technical University, Munich, Germany
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Caroline Böttiger
- Experimental Neurology, Department of Neurology and Center for Stroke Research, Charité, Berlin, Germany
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Martina Füchtemeier
- Experimental Neurology, Department of Neurology and Center for Stroke Research, Charité, Berlin, Germany
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Plamena Stroh
- Experimental Neurosurgery, Department of Neurosurgery, Klinikum rechts der Isar, Technical University, Munich, Germany
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Christoph Leithner
- Experimental Neurology, Department of Neurology and Center for Stroke Research, Charité, Berlin, Germany
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Georg Royl
- Experimental Neurology, Department of Neurology and Center for Stroke Research, Charité, Berlin, Germany
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Ulrich Dirnagl
- Experimental Neurology, Department of Neurology and Center for Stroke Research, Charité, Berlin, Germany
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Nikolas Offenhauser
- Experimental Neurology, Department of Neurology and Center for Stroke Research, Charité, Berlin, Germany
| Published: | September 16, 2010 |
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Outline
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Objective: Within the first hours after cortical spreading depression (CSD) moderate hypoperfusion with impaired vascular reactivity occurs. However, it is not investigated in detail, whether the observed alteration of cerebrovascular reactivity has any impact on neurovascular and neurometabolic coupling.
Methods: Rats were anesthetized with isoflurane in N_2O/O_2, mechanically ventilated and equipped with a cranial window. Systemic blood pressure, body temperature and arterial blood gases were controlled and kept within physiological limits. After surgery, anesthesia was changed to i.v. chloralose/urethane. A single CSD was elicited by pin prick at a small burr hole rostral from the cranial window. Cerebral blood flow (CBF) and cerebral blood oxygenation (CBO) was measured with combined laser Doppler flowmetry and optical spectroscopy. BOLD-fMRI was performed in animals without cranial window preparation, using a Bruker 7T PharmaScan. Somatosensory stimulation was induced by whisker hair deflection or electrical forepaw stimulation. EEG and SEPs were recorded by a silver ball surface electrode. In separate animals, brain tissue content of glucose, lactate and glycogen were measured up to 90 minutes following CSD.
Results: Within the first 30 minutes after CSD, the CBF response to whisker deflection was significantly reduced by 39±29% (p<0.05) with only minor reduction of the neuronal response. Under these conditions the deoxy-Hb response was considerably altered to both whisker and forepaw stimulation, showing a biphasic pattern with a pronounced initial increase at stimulation onset. During the observation period of 90 minutes, the deoxy-Hb response remained altered despite slow recovery of resting CBF and of CBF response to functional activation. Tissue glycogen almost disappeared 15 minutes after CSD, and slowly recovered but was still slightly reduced 90 minutes after CSD.
Conclusions: The altered CBO response following CSD cannot solely be explained by impaired cerebrovascular reactivity, and changes in cerebral metabolism seem to occur in parallel. Increased baseline oxygen metabolism and reduced CBF during resting and stimulation conditions after CSD was recently also demonstrated by Piilgaard and Lauritzen (J Cereb Blood Flow Metab, 2009). These combined vascular and metabolic changes after CSD can be considered as a possible cause for the altered deoxy-Hb response shown in our experiments.
