# Pulmonary edema following subarachnoid hemorrhage is associated with impairment of pulmonary vascular endothelial glycocalyx

## TL;DR

This study shows that lung fluid buildup after brain hemorrhage is linked to damage in the lung's blood vessel lining, suggesting a new target for treatment.

## Contribution

The study identifies pulmonary endothelial glycocalyx impairment as a novel mechanism underlying neurogenic pulmonary edema after subarachnoid hemorrhage.

## Key findings

- Lung water content was significantly increased in SAH mice compared to sham controls.
- Scanning electron microscopy revealed severe glycocalyx damage in SAH mice.
- Tomato lectin fluorescence intensity was significantly reduced in SAH mice, indicating PEG loss.

## Abstract

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.

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.