gms | German Medical Science

Objective: The neuroprotective effect of argon after experimental subarachnoid hemorrhage (SAH) has already been demonstrated evaluating the hippocampal region 24h after SAH. Here, we examine the hippocampal region and further cerebral areas with regard to neuronal damage and microglia activation 6 and 72h after SAH.

Methods: Experimental subarachnoid hemorrhage (Sprague Dawley rats) was carried out in n=27 rats applying the endovascular perforation model. One hour after subarachnoid hemorrhage or sham surgery, a breathing gas mixture containing 50 vol% argon/50 vol% oxygen (argon group) or 50 vol% nitrogen/50 vol% oxygen (control group) was applied for 1 hour. Cerebral coronal H&E stained sections were selected for assessment of histological neuronal cell damage in nine predefined anatomical regions of interest (ROIs) with 5 ROIs in the left hippocampus and 4 ROIs in the left cortex. In addition microglial activation was evaluated by a cell count of activated microglia in Iba-1 stained slices. For statistical analysis dependent on normality, testing unpaired t-test or Mann-Whitney U test were applied. For group comparisons, one-way ANOVA followed by post hoc testing was performed.

Results: When the hippocampal regions 6h after SAH were compared, there was a significantly reduced neuronal damage in the argon group (37±16 vs. 60±25 %; p<.05). This effect was particularly pronounced in the CA2, CA2/3 and CA3 region (p<.05). 72h after SAH a still significant, but less pronounced reduction regarding hippocampal neuronal cell death was found in the argon-treated animals comparing the SAH groups (33±14 vs. 47±17%; p<.05). This effect was now only particularly pronounced in the CA3 region (p<.05). However, cortical cell loss was also seen to be reduced in the PLCo area after argon treatment. Microglia activation increased with time. A trend towards less microglia activation in the argon treated group was seen.

Conclusion: Here, we demonstrate the neuroprotective effect of argon after experimental SAH especially in hippocampal regions. The early pronunciation of this effect could be due to a lack of sustainability. Further, regions affected vary considerably between the experiments and the samples of sham treated animals show a noticeable tissue damage. Thus, sample size has to be increased to verify this finding.