Artikel
A systematic and meta-analysis of mortality in experimental mouse models analyzing delayed cerebral ischemia after subarachnoid hemorrhage
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Autoren
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Jasmin Weber
- Department of Neurosurgery, Medical Faculty, Heinrich Heine University, Düsseldorf, Deutschland
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Igor Fischer
- Division of Informatics and Statistics, Department of Neurosurgery, Medical Faculty, Heinrich Heine University, Düsseldorf, Deutschland
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Jasper H. V. Lieshout
- Department of Neurosurgery, Medical Faculty, Heinrich Heine University, Düsseldorf, Deutschland
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Tanja Restin
- Institute of Physiology, Zurich Centre of Integrative Human Physiology, University of Zurich, Institute of Anesthesiology, University Hospital Zurich, Zurich, Switzerland
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Hans-Jakob Steiger
- Universitätsklinikum Düsseldorf, Neurochirurgische Klinik, Düsseldorf, Deutschland
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Marcel Alexander Kamp
- Department of Neurosurgery, Medical Faculty, Heinrich Heine University, Düsseldorf, Deutschland
| Veröffentlicht: | 9. Juni 2017 |
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Gliederung
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Objective: Mouse models are established models to study pathophysiological changes following subarachnoid hemorrhage (SAH) and remodel the human situation. The aim of the present systematic analysis was to determine the mortality rate in mouse SAH models of delayed cerebral ischemia (DCI), to identify factors influencing mouse mortality and to compare mouse mortality to the case fatality in human SAH patients.
Methods: A systematic search of the PubMed database was performed to identify all studies that assessed mouse DCI models. Mortality rates and predictor variables were extracted and compared to previously reported human case fatality after SAH. The Kruskal-Wallis test was used for all questions including more than two classes and the Wilcoxon rank sum test with continuity correction was used to compare mortality between mouse DCI models and SAH patients. As multiple statistical testing was performed, a level of less than 0.0021 was considered to be significant according to Šidák´s correction.
Results: Forty-eight studies were included in the quantitative analysis. The mean overall mortality rate was 21% in mouse DCI models. The time period between induction of SAH and evaluation of mortality rates is a significant variable influencing the mortality rate in mouse SAH models. Furthermore, the mouse mortality after 48 hours rate was significantly influenced by the used SAH model (injection vs. endovascular perforation model). In contrast, neither the genetic background nor the anesthetic had a significant effect on the case fatality rate. Mouse mortality after experimental SAH in DCI models was significant lower than human case fatality following aneurysmal SAH.
Conclusion: The mean overall mortality rate in mouse DCI models is significantly lower than human case fatality following aneurysmal SAH. However, time between SAH induction and evaluation is a significant variable influencing the mortality rate in mouse SAH models. Further analyses will be required to establish whether and to which extent different DCI models affect mortality and reflect human pathophysiology.
