gms | German Medical Science

Objective: The molecular pathways underlying their pathogenesis of vasospasms and delayed cerebral ischemia (DCI) after subarachnoid hemorrhage remain poorly understood. Using the murine single injection model, we examined the effects of SAH on regional cerebral blood flow in the somatosensory cortex (S1) and cerebellar cortex, neurobehavioural integrity and changes in electrocorticography and histopathological morphology.

Method: Totally, 80 C57BL/6J mice were analyzed. After induction of general anesthesia, 50 µl freshly-drawn blood obtained from the tail vein (or saline for the saline injection group or no injection but perforation of the atlanto-occipital membrane for the sham group) was injected in the cisterna magna. Relative rCBF was evaluated by Laser-Dopplermetry above the S1 and the cerebellar cortex and data were collected 10 minutes before and 10 minutes at the endpoints 0, 6, 12, 24, 72 hours after SAH. Telemetric electrocorticograms from the S1 and cerebellar cortex recorded by implanted transmitters were continuously collected and were used to calculate absolute and relative power of frequency bands. A neuro-behavioral evaluation was performed at 12, 24, 72 hours after SAH.

Results: Totally, 80 mice's were analyzed. Mortality rate group was 15.2% in the SAH and 0% in the saline injection and sham group. Animals in the SAH group displayed significant deficits in sensory tests compared to the sham and saline injection group 12 hours and 24 hours after SAH. SAH animals displayed a significant decrease of rCBF of S1 compared to the saline injected animals after 6, 12 and 24 hours and compared to the sham operated animals after 6 and 12 hours after injection. Cerebellar rCBF and Conc was significantly reduced compared to both control groups after 6 and 12 hours. rCBF reestablished after 3 days in all groups. SAH animals displayed significantly increased absolute delta power i.e. slowing 12 hours and 24 hours after SAH reflected by a reduction in alpha/delta ratio (ADR) compared to saline-injected animals 24 hours after SAH. Periodically recurring short episodes of depression of activity within the 0.5 – 2 Hz range lasting 2-3 seconds were observed in some SAH animals but not in saline-injected or sham-operated animals reflecting spreading depolarizations. After 3 days, no differences in ECoG spectra were visible between the three groups.

Conclusions: The murine blood injection SAH model is suitable to evaluate pathophysiological analysis of DCI following SAH.