increasing vascularity. This study tested whether sevoflurane postconditioning would improve long-term neurologic deficit through increased formation of new vessels close to the hemorrhage area. METHODS: Fifty-three animals were subjected to SAH or sham surgery with or without a 2-hour sevoflurane postconditioning (versus propofol anesthesia). Animal survival, including dropout animals due to death or reaching termination criteria, as well as neurologic deficit, defined by the Garcia score, were assessed 2 hours after recovery until postoperative day 14. On day 14, blood samples and brain tissue were harvested. Vessel density was determined by the number of cluster of differentiation 31 (CD31)–positive vessels, and activated glial cells by glial fibrillary acidic protein (GFAP)–positive astrocytes per field of view. RESULTS: The survival rate for sham animals was 100%, 69% in the SAH-propofol and 92% in the SAH-sevoflurane groups. According to the log-rank Mantel-Cox test, survival curves were significantly different (P = .024). The short-term neurologic deficit was higher in SAH-propofol versus SAH-sevoflurane animals 2 hours after recovery and on postoperative day 1 (propofol versus sevoflurane: 14. 6 ± 3.4 vs 15. 9 ± 2.7 points, P = .034, and 16. 2 ± 3.5 vs 17. 8 ± 0.9 points, P = .015). Overall complete recovery from neurologic deficit was observed on day 7 in both SAH groups (18. 0 ± 0.0 vs 18. 0 ± 0.0 points, P = 1.000). Cortical vascular density increased to 80. 6 ± 15.0 vessels per field of view in SAH-propofol animals (vs 71. 4 ± 10.1 in SAH-sevoflurane, P < .001). Activation of glial cells, an indicator of neuroinflammation, was assessed by GFAP-positive astrocytes GFAP per field of view. Hippocampal GFAP-positive cells were 201 ± 68 vs 179 ± 84 cells per field of view in SAH-propofol versus SAH-sevoflurane animals (P < .001). CONCLUSIONS: Sevoflurane postconditioning improves survival by 23% (SAH-sevoflurane versus SAH-propofol). The sevoflurane intervention could attenuate the early neurologic deficit, while the long-term outcome was similar across the groups. A higher vascular density close to the SAH area in the propofol group was not associated with improved outcomes....

中文翻译：

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七氟烷后处理可防止蛛网膜下腔出血后的早期神经功能缺损：大鼠随机实验室研究的结果


血管分布增加。本研究测试了七氟烷后处理是否会通过增加出血区域附近新血管的形成来改善长期神经功能缺损。方法： 53 只动物接受 SAH 或假手术，有或没有 2 小时七氟烷后处理 （与丙泊酚麻醉相比）。在恢复后 2 小时至术后第 14 天评估动物存活率，包括因死亡或达到终止标准而退出的动物，以及由 Garcia 评分定义的神经功能缺损。第 14 天，采集血样和脑组织。血管密度由分化簇 31 （CD31） 阳性血管的数量决定，活化的神经胶质细胞由神经胶质纤维酸性蛋白 （GFAP） 阳性星形胶质细胞决定。结果： 假动物的存活率为 100%，SAH-异丙酚组为 69%，SAH-七氟烷组为 92%。根据对数秩 Mantel-Cox 检验，生存曲线显著不同 （P = .024）。在恢复后 2 小时和术后第 1 天，SAH-异丙酚与 SAH-七氟烷动物的短期神经功能缺损更高（异丙酚与七氟烷：14. 6 ± 3.4 对 15. 9 ± 2.7 分，P = .034，和 16. 2 ± 3.5 对 17.8 ± 0.9 分，P = .015）。在第 7 天观察到两个 SAH 组的神经功能缺损总体完全恢复 （18. 0 ± 0.0 vs 18. 0 ± 0.0 分，P = 1.000）。皮质血管密度增加到 80。6 ± SAH-异丙酚动物每个视野 15.0 个血管（与 SAH-七氟烷相比 71.4 ± 10.1，P < .001）。神经胶质细胞的激活是神经炎症的一个指标，通过每个视野的 GFAP 阳性星形胶质细胞 GFAP 进行评估。 SAH-异丙酚与 SAH-七氟烷动物的海马 GFAP 阳性细胞分别为 201 ± 68 个细胞对 179 ± 84 个细胞 （P < .001）。结论： 七氟烷后处理使生存率提高了 23% （SAH-七氟烷与 SAH-丙泊酚）。七氟烷干预可以减轻早期神经功能缺损，而各组的长期结局相似。丙泊酚组靠近 SAH 区域的较高血管密度与改善的结果无关。