Capillary flow disturbances after experimental subarachnoid hemorrhage: A contributor to delayed cerebral ischemia?

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.

To investigate capillary flow changes 4 days following experimental SAH.

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.

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.

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.