gms | German Medical Science

Objective: Delayed vasospasm and delayed cerebral infarction are well-known sequelae after subarachnoid hemorrhage (SAH). Acute vasospasm has been postulated due to a discrepancy between quickly recovering cerebral vasospasm and long-lasting reduction of cerebral blood flow (CBF) in the first hours after SAH. To date, however, the onset and development of early vasospasm have not been visualized and are not completely understood. It was the aim of this study to visualize the changes of the cerebral vasculature before, during and in the first hours after experimental SAH using in vivo video microscopy of cortical vessels and the cortical surface.

Methods: Male Sprague-Dawley rats were assigned to either undergo experimental SAH using the endovascular filament model or a sham operation (n = 10). Local CBF was continuously measured using laser-Doppler flowmetry over the left frontal cortex. Mean arterial blood pressure and arterial blood gases were measured continuously. In vivo video microscopy (XCSource^® USB 20-800x) of cortical vessels was performed through a cranial window (d = 3 mm) over the right fronto-parietal cortex. Video files and photographs were obtained before, during and 5, 30, 60, 120 and 180 minutes after SAH. Vessel diameter in predefined regions of interest was measured using AMCAP-Software and assessed with GraphPad PRISM software.

Results: During and in the first seconds after SAH, arterial vessels completely disappeared and slowly reappeared over the following minutes. In the following 3 hours, disperse focal vasospasms were seen in all parts of the visible areas of the cerebral vasculature. Vessel diameter decreased significantly in the regions of interest in all animals subjected to SAH. Small subarachnoid vessels were ls after SAH, No changes were observed in the sham-operated group at any time point. Mean vessel diameter in regions of interest significantly decreased after SAH. Interestingly, some vessels seem to recover after a while and re-contract later in other vessel sections.

Conclusion: For the first time, in vivo development/formation of vasospasm after SAH was shown. In contrast to delayed vasospasm onset after 48 – 72 hours, we see acute vasospasm/vasoconstriction after SAH which may lead to early secondary brain damage and ischemia. Further investigation is necessary to identify possible treatment options for early onset vasospasm.