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Acta Neurochir. Suppl. · Jan 2011
Subarachnoid hemorrhage causes pulmonary endothelial cell apoptosis and neurogenic pulmonary edema in mice.
- Hidenori Suzuki, Takumi Sozen, Yu Hasegawa, Wanqiu Chen, Kenji Kanamaru, Waro Taki, and John H Zhang.
- Department of Neurosurgery, Mie University Graduate School of Medicine, Tsu, Japan.
- Acta Neurochir. Suppl. 2011 Jan 1;111:129-32.
ObjectsNeurogenic pulmonary edema (NPE) is a well-known complication of subarachnoid hemorrhage (SAH), which potentially causes a poor outcome. The aim of this study was to examine if NPE occurs in the endovascular perforation model of SAH in mice and if apoptosis contributes to NPE development after SAH in mice.MethodsSham-operated or SAH mice were treated with an intraperitoneal administration of vehicle or an antiapoptotic drug Z-Val-Ala-Asp-fluoromethylketone (Z-VAD-FMK) 1 h post-SAH. Pulmonary edema measurements and evaluation of apoptosis occurrence were performed on the lung at 24 h post-SAH.ResultsSAH caused NPE, which was associated with apoptosis of pulmonary endothelial cells. Z-VAD-FMK significantly prevented apoptosis and NPE.ConclusionsPulmonary endothelial cell apoptosis contributes to the pathophysiology of NPE after SAH in mice.
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