Artikel
Characterization of cerebral autoregulation in the acute phase after experimental subarachnoid hemorrhage
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Autoren
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Catharina Conzen
- RWTH Aachen, Klinik für Neurochirurgie, Aachen, Deutschland
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Walid Albanna
- RWTH Aachen, Klinik für Neurochirurgie, Aachen, Deutschland
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Katrin Becker
- RWTH Aachen, Klinik für Neurochirurgie, Aachen, Deutschland
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Annika Bach
- RWTH Aachen, Klinik für Neurochirurgie, Aachen, Deutschland
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Ute Lindauer
- RWTH Aachen, Klinik für Neurochirurgie, Aachen, Deutschland
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Hans Clusmann
- RWTH Aachen, Klinik für Neurochirurgie, Aachen, Deutschland
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Gerrit Alexander Schubert
- RWTH Aachen, Klinik für Neurochirurgie, Aachen, Deutschland
| Veröffentlicht: | 18. Juni 2018 |
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Gliederung
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Objective: Delayed disturbances of cerebral autoregulation (CA) after aneurysmal subarachnoid hemorrhage (SAH) correlate with unfavorable neurological outcome, but data about the acute phase and the involved mechanisms are scarce. This study aims to determine the role of initial intracranial hypertension (iHTN) and injection composition (blood vs saline) regarding disturbances of CA in the acute phase after experimental SAH.
Methods: SAH in 48 rats was induced by cisternal injection of 0.5ml of arterial blood (B) or normal saline (S) in predefined time frames: B1:1min, B10:10min, B30:30min, S1:1 min, S10:10min. Regional cortical blood flow, intracranial pressure (ICP) and mean arterial blood pressure (mABP) were recorded for 6 h after SAH. CA was assessed using the moving correlation coefficient between ICP and mABP, the pressure reactivity index (PRx); values >0.2 indicate impaired CA.
Results: Rapid injection velocity (B1, B10) resulted in a more pronounced increase in ICP (B1 vs B10 p<0.05, B1 vs B30 p<0.001, B10 vs B30 p=0.08, S1 vs S10 p<0.001). B1 showed significantly higher ICP increases compared to S1 (p<0.01) initially and throughout the observation period (p<0.01). While CA was intact in all groups before injection, B1 and B10 showed significant disruption of PRx acutely (p<0.05; average 15-20min), followed by rapid normalization. A secondary worsening of CA was observed in B1 and then persisted throughout the rest of the experiment. B10 showed a fluctuating course, intermittently exceeding the critical threshold.
S1 showed a non-significant increase in PRx (p=0.07), with fast recovery after 30min. PRx was unaffected in S10. In B30, PRx was preserved initially, but disruption of CA occurred at completion of injection (37 min: p<0.001) followed by recovery thereafter.
Conclusion: Disturbances of CA occur in the hyperacute phase after experimental SAH. Impairment shortly after injection was detectable in all hemorrhage groups and in the rapid NS injection group followed by fast recovery. Secondary worsening of CA within the first hours after SAH was identified as a characteristic feature within rapid hemorrhagic injection groups.
As iHTN was most pronounced in these groups, both severity of iHTN (determined by injection velocity) and composition (hemorrhage) are plausible contributors to secondary, but early impairment of CA.
