Artikel
Patterns of death in experimental subarachnoidal hemorrhage
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Autoren
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Maxine Dibué-Adjei
- Neurochirurgische Klinik, Heinrich-Heine-Universität, Düsseldorf, Germany; Institut für Neurophysiologie, Universität zu Köln, Germany; Zentrum für Molekulare Medizin Köln, Germany
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Carolin Dietrich
- Neurochirurgische Klinik, Heinrich-Heine-Universität, Düsseldorf, Germany
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Hans-Jakob Steiger
- Neurochirurgische Klinik, Heinrich-Heine-Universität, Düsseldorf, Germany
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Toni Schneider
- Institut für Neurophysiologie, Universität zu Köln, Germany; Zentrum für Molekulare Medizin Köln, Germany
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Daniel Hänggi
- Neurochirurgische Klinik, Heinrich-Heine-Universität, Düsseldorf, Germany; Neurochirurgische Klinik, Universitätsmedizin Mannheim, Medizinische Fakultät Mannheim der Universität Heidelberg, Germany
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Marcel A. Kamp
- Neurochirurgische Klinik, Heinrich-Heine-Universität, Düsseldorf, Germany; Institut für Neurophysiologie, Universität zu Köln, Germany
| Veröffentlicht: | 8. Juni 2016 |
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Gliederung
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Objective: In addition to delayed cerebral ischemia (DCI), early brain injury (EBI) is a major factor contributing to high mortality following SAH. Animals dying after experimental SAH are usually excluded from further analysis. Therefore, reasons of early case fatality are rarely studied but could be of great value, as the pathophysiological mechanisms of early death following SAH in humans remain unknown. Therefore, we analyzed cerebral perfusion and cortical signaling in mice that died due to experimental SAH.
Method: SAH was induced by injection of 50 µl freshly-drawn blood into the cisterna magna. Relative cerebellar and cerebral regional cerebral blood flow (rCBF) was evaluated by laser-doppler flowmetry before and after induction of SAH and at the time point before mice were killed for further analysis. Telemetric electrocorticograms (ECoG) from the S1 cortex recorded by implanted transmitters were continuously collected and were used to calculate absolute and relative power of frequency bands.
Results: Totally, 59 mice were subjected to experimental SAH (50 native mice backcrossed 4x in C57Bl/6, leaving behind some 129SvJ-background and 9 Cav2.3-deficient mice). Totally, 9 mice died following SAH induction (mortality rate: 15.2%; 14% of the Cav2.3 +/+ and 22.2% of the Cav2.3 -/-). One mouse died one hour after SAH induction and 8/9 mice immediately after SAH induction. For the mice died within the first minutes, SAH induction immediately leads to complete cessation cerebral perfusion and total ECoG power. This pattern was also observed in mice that survived SAH induction, however in contrast to mice died, rCBF recovered within 5 minutes and subsequently cortical signaling within 10 minutes.
Conclusions: In the murine SAH-injection model, EBI with initial complete rCBF reduction and disruption of cortical signaling is the major component contributing to SAH-related mortality. Further studies may further evaluate this very early phase following SAH to investigate why rCBF does recover in some animals but not in all. However, this ultra-early phase following SAH is rarely accessible for a directed therapeutic approach.
