Localized pulmonary vascular changes in a mouse model of subarachnoid hemorrhage created by combining filament perforation and blood injection.

INTRODUCTION

Subarachnoid hemorrhage (SAH) results in neurogenic pulmonary edema (NPE), a condition with a high mortality rate arising from increased hydrostatic pressure and vascular permeability. Two possible mechanisms of NPE are increased hydrostatic pressure and increased vascular permeability, and it is possible that increased permeability of capillaries in the lungs may contribute to the exacerbation of NPE. Recent research has highlighted the importance of the glycocalyx, a gel-like layer that lines blood vessels, in regulating vascular permeability in various diseases. However, its role in NPE after SAH has not been previously explored. This study investigated the involvement of the glycocalyx in the development of NPE by developing a mouse model of SAH.

METHODS

The SAH model was developed by combining internal carotid artery (ICA) perforation and blood infusion into the cisterna magna of mice. The histological structure of the lungs was confirmed using micro-CT, histopathological examination, and scanning electron microscopy.

RESULTS

Despite no obvious micro-CT findings indicating pulmonary edema, histopathological changes in hematoxylin and eosin-stained lung were detected. Scanning electron microscopy revealed glycocalyx exfoliation within the pulmonary microvascular wall. A trend toward higher plasma syndecan-1 levels was also observed.

CONCLUSION

The combination of ICA perforation and blood infusion into the cisterna magna can produce pulmonary findings in mice that mimic NPE after SAH. The results also suggest that glycocalyx loss is involved in the development of NPE after SAH.