Key result
Subarachnoid hemorrhage increases lung water content by ~3 percentage points vs sham in mice.
Why the study?
Neurogenic pulmonary edema often occurs after aneurysmal subarachnoid hemorrhage, but the mechanism of its progression remains unclear.
Does experimental subarachnoid hemorrhage cause neurogenic pulmonary edema and impairment of pulmonary vascular endothelial glycocalyx in a mouse model?
Does experimental subarachnoid hemorrhage cause neurogenic pulmonary edema and impairment of pulmonary vascular endothelial glycocalyx in a mouse model?
Absolute Event Rate: 81.7% vs 78.8%
p-value: p=0.007
This preclinical study demonstrates that neurogenic pulmonary edema following subarachnoid hemorrhage is associated with the degradation and shedding of the pulmonary vascular endothelial glycocalyx.
May support glycocalyx-targeted research in neurogenic pulmonary edema; leaves open translation from this mouse model to clinical practice.
Although neurogenic pulmonary edema (NPE) often occurs after aneurysmal subarachnoid hemorrhage (SAH), the mechanism of NPE progression after SAH remains unclear. This study investigates whether pulmonary endothelial glycocalyx (PEG) impairment accompanies NPE after SAH. Accordingly, SAH was induced by endovascular perforation in male mice. The lung tissues of the mice were removed 24 h after SAH induction. The degree of pulmonary edema and lung injury, and the extent of PEG injury were assessed. Water content of lung tissue by the wet/dry method in the SAH group was significantly increased compared to that in the sham group (81.7 % vs. 78.8 %, P < 0.01), which suggested NPE following SAH. Lung injury score by hematoxylin and eosin staining in the SAH group, assessed using a semiquantitative scoring system, was also significantly worse than that in the sham group (7.1 vs. 1.2, P < 0.001). Scanning electron microscopy images clearly demonstrated that the moss-like glycocalyx lined the endothelial lumen without any interruption in sham mice, whereas those microstructures were severely devastated in SAH mice. Moreover, the fluorescence intensity of tomato lectin was significantly reduced in SAH mice compared to that in sham mice (13.3 vs. 30.7, P < 0.001), thereby indicating the loss of PEG. Our results indicate that PEG, which is essential for regulating vascular permeability, is severely impaired after experimental SAH. Maintaining the integrity of PEG is a promising therapeutic strategy for NPE after SAH. • SAH worsens lung water content and histopathological findings. • Shedding of PEG after SAH is associated with the mechanism of pulmonary edema. • Shedding of PEG was observed using SEM and quantified by tomato lectin staining.
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Sasaki et al. (2025) studied Subarachnoid hemorrhage (neurogenic pulmonary edema) (n=37). Subarachnoid hemorrhage induction via endovascular perforation vs. Sham procedure was evaluated on Water content of lung tissue (95% CI -4.86 to -0.97, p=0.007). Experimental subarachnoid hemorrhage in mice significantly increased lung tissue water content compared to a sham procedure (81.7% vs 78.8%), accompanying pulmonary endothelial glycocalyx impairment.
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