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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Amino Acid Chloromethyl Ketones, Analysis of Variance, Animals, Apoptosis, Caspase 3, Disease Models, Animal, Endothelial Cells, In Situ Nick-End Labeling, Indoles, Lung, Mice, Neuroprotective Agents, Pulmonary Edema, Subarachnoid Hemorrhage, von Willebrand Factor.
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Does subarachnoid hemorrhage cause pulmonary endothelial cell apoptosis and neurogenic pulmonary edema in mice? Context: Neurogenic 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. Sham-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. SAH caused NPE, which was associated with apoptosis of pulmonary endothelial cells. Z-VAD-FMK significantly prevented apoptosis and NPE.
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Pulmonary endothelial cell apoptosis contributes to the pathophysiology of NPE after SAH in mice. Final Decision: yes