Artikel
The effect of ketamine on vascular reactivity during spreading depolarization in gyrencephalic swine cortex
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Autoren
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Renán Sánchez-Porras
- Department of Neurosurgery, University Hospital Heidelberg, Heidelberg, Germany
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Edgar Santos
- Department of Neurosurgery, University Hospital Heidelberg, Heidelberg, Germany
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Michael Schöll
- Department of Neurosurgery, University Hospital Heidelberg, Heidelberg, Germany; Institute of Medical Biometry and Informatics, Ruprecht Karls University, Heidelberg, Germany
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Christian Stock
- Institute of Medical Biometry and Informatics, Ruprecht Karls University, Heidelberg, Germany
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Yuan Gang
- Department of Neurosurgery, University Hospital Heidelberg, Heidelberg, Germany; Department of Neurosurgery, The First Hospital, Jilin University, China
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Zelong Zheng
- Department of Neurosurgery, University Hospital Heidelberg, Heidelberg, Germany
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Patrick Schiebel
- Department of Neurosurgery, University Hospital Heidelberg, Heidelberg, Germany
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Berk Orakcioglu
- Department of Neurosurgery, University Hospital Heidelberg, Heidelberg, Germany
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Andreas W. Unterberg
- Department of Neurosurgery, University Hospital Heidelberg, Heidelberg, Germany
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Oliver W. Sakowitz
- Department of Neurosurgery, University Hospital Heidelberg, Heidelberg, Germany
| Veröffentlicht: | 13. Mai 2014 |
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Gliederung
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Objective: Spreading depolarization (SD) is a wave of mass neuronal and glial cell depolarization. SD is associcated with profound cerebrovascular changes that may have important clinical consequences. Ketamine, a NMDA receptor blocker, has the capacity to modify SD occurrence. However, the studies addressing its influence on cerebral hemodynamics are still controversial. The aim of this study was to analyze the effect of ketamine on vascular reactivity during SD occurrence through intrinsic optical signal (IOS) imaging in a gyrencephalic swine brain.
Method: Five male swine were craniotomized and an image acquisition system with a camera was mounted 25 cm above the exposed hemisphere for IOS imaging. SDs were induced with a small drop (1-3 microL) of KCl (1 mmol/ml) every 30 min for a total of 12 stimulations. An infusion of 2 mg/kg/h ketamine (Ketanest S® 25 mg/ml) was perfused for 2 h from the 5-9th stimulation. Two cerebral arteries from each hemisphere were selected for diameter changes and SD analysis.
Results: We identified two distinct patterns of vascular reactivity during SD occurrence before ketamine administration. The first pattern consisted of biphasic (50%) vasomotor changes with a vasodilation (41.7 ± 19.9%, mean ± STD) and vasoconstriction (13.6 ± 11.9%). A second pattern of triphasic (30%) vasomotor components with a vasoconstriction (19.9 ± 9.0%), vasodilation (35.2 ± 19.7%) and vasoconstriction (15.6 ± 12.9%) was found. During infusion of 2 mg/kg/h ketamine vascular responses were affected. The biphasic pattern exhibited a reduction of 18.2% for the dilative phase and an increase of 0.2% in the constrictive phase. In the case of the triphasic pattern, there was a reduction of 4.5% for the first vasoconstriction; the dilative phase showed a reduction of 27.5% and the second vasoconstrictive phase was not affected. The duration of these patterns also showed reductions during ketamine administration.
Conclusions: Vascular reactivity is impaired after SD. Our preliminary data indicate that ketamine exerted a stabilizing effect over vascular responses during SD on cerebral arteries.
