Maryam Anzabi1, Hugo Angleys1, Rasmus Aamand1, Maryam Ardalan1,2, Kim Mouridsen1, Peter Mondrup Rasmussen1, Jens Christian Hedemann Sørensen3, Nikolaus Plesnila4, Leif Østergaard1,5, Nina Kerting Iversen1. 1. Department of Clinical Medicine, Center of Functionally Integrative Neuroscience (CFIN), Aarhus University, Aarhus, Denmark. 2. Department of Clinical Medicine, Translational Neuropsychiatry Unit, Aarhus University, Aarhus, Denmark. 3. Department of Neurosurgery, Department of Clinical Medicine, Aarhus University and Aarhus University Hospital, Aarhus, Denmark. 4. Institute for Stroke and Dementia Research (ISD), University of Munich Medical Center, Munich, Germany. 5. Department of Neuroradiology, Aarhus University Hospital, Aarhus, Denmark.
Abstract
BACKGROUND: The high mortality and morbidity after SAH is partly due to DCI, which is traditionally ascribed to development of angiographic vasospasms. This relation has been challenged, and capillary flow disturbances are proposed as another mechanism contributing to brain damage after SAH. OBJECTIVE: To investigate capillary flow changes 4 days following experimental SAH. METHODS: SAH was induced by endovascular perforation of circle of Willis. We used TPM to evaluate blood flow characteristics. Cortical capillary diameters were investigated by both TPM and histology. RESULTS: We found elevated CTH and MTT of blood in SAH mice compared to sham animals. We observed capillaries with stagnant RBCs, and capillaries with increased RBC LD in the SAH group, suggesting severe blood maldistribution among cortical capillaries. Favoring that these capillary flow changes were primary to upstream vasoconstrictions, TPM showed no significant differences in arteriolar diameter between groups, while histological examination showed reduced capillary diameter in SAH group. CONCLUSION: Our study shows profound subacute hypoperfusion and capillary flow disturbances in a mouse SAH model and suggests that these changes are the result of changes in capillary function, rather than upstream vasospasm.
BACKGROUND: The high mortality and morbidity after SAH is partly due to DCI, which is traditionally ascribed to development of angiographic vasospasms. This relation has been challenged, and capillary flow disturbances are proposed as another mechanism contributing to brain damage after SAH. OBJECTIVE: To investigate capillary flow changes 4 days following experimental SAH. METHODS:SAH was induced by endovascular perforation of circle of Willis. We used TPM to evaluate blood flow characteristics. Cortical capillary diameters were investigated by both TPM and histology. RESULTS: We found elevated CTH and MTT of blood in SAHmice compared to sham animals. We observed capillaries with stagnant RBCs, and capillaries with increased RBC LD in the SAH group, suggesting severe blood maldistribution among cortical capillaries. Favoring that these capillary flow changes were primary to upstream vasoconstrictions, TPM showed no significant differences in arteriolar diameter between groups, while histological examination showed reduced capillary diameter in SAH group. CONCLUSION: Our study shows profound subacute hypoperfusion and capillary flow disturbances in a mouseSAH model and suggests that these changes are the result of changes in capillary function, rather than upstream vasospasm.
Authors: B B Hofmann; I Fischer; A Engel; K Jannusch; D M Donaldson; C Karadag; J H van Lieshout; K Beseoglu; S Muhammad; B Turowski; D Hänggi; M A Kamp; C Rubbert Journal: AJNR Am J Neuroradiol Date: 2021-06-03 Impact factor: 4.966
Authors: Tobias P Schmidt; Walid Albanna; Miriam Weiss; Michael Veldeman; Catharina Conzen; Omid Nikoubashman; Christian Blume; Daniel S Kluger; Hans Clusmann; Sven H Loosen; Gerrit A Schubert Journal: Front Neurol Date: 2022-03-10 Impact factor: 4.003