通过双侧颈总动脉结扎在兔体内血流动力学诱导颅内动脉瘤：一项系统综述与荟萃分析。
完整摘要 · 中文译文
背景/目的：兔双侧颈总动脉结扎（BCCAL）模型用于模拟血流动力学驱动的颅内动脉瘤形成。然而，报告不一致和终点异质性掩盖了其基线疗效。本系统评价和荟萃分析确定了动脉瘤诱导的合并发生率，并绘制了相关结构和血流动力学变化的时序进展。 方法：检索PubMed、Embase和Web of Science（截至2026年9月5日），纳入实施BCCAL模型的实验研究。使用随机效应广义线性混合模型（GLMM）评估肉眼可见的动脉瘤形成。对于破坏性动脉瘤重塑，由于事件率均一，GLMM在统计学上不适用，故采用精确二项比例进行评估。次要结局（死亡率、血流动力学和病理组织学降解）采用单臂连续、比较二分类和多水平混合效应荟萃分析进行评估，并在存在重复测量时进行聚类稳健敏感性分析。 结果：在纳入的22项研究中，肉眼可见动脉瘤形成的合并发生率为23.4%（k = 3项研究），而破坏性结构损伤在所有接受该结局评估的动物中均有报告，尽管其操作定义在各研究间有所不同。与假手术对照组相比，BCCAL将绝对死亡风险增加了16.6%。急性期（1至7天），基底动脉血流速度和壁面剪切应力显著升高，同时伴有快速的内弹性膜（IEL）破坏。 离子（平均间隙507.34 µm）及中膜变薄（450.32 µm）。血流速率亦增加，尽管该趋势在聚类稳健敏感性分析中未得以维持。在慢性期（>7天），代偿性血管扩张减弱了局部血流动力学应力。结构缺损此后是否保持稳定或进一步进展，尚无法确切判定。 结论：兔BCCAL模型通过快速机械性损伤可靠地诱导早期动脉瘤样重构，但其长期结构演变轨迹仍未明确。本研究提供了初步的发病率和死亡率估计，有助于为未来临床前神经血管试验的样本量和效能计算提供参考。
完整摘要 · 英文原文
BACKGROUND/OBJECTIVES: The rabbit bilateral common carotid artery ligation (BCCAL) model is utilized to simulate hemodynamically driven intracranial aneurysm formation. However, inconsistent reporting and heterogeneous endpoints obscure its baseline efficacy. This systematic review and meta-analysis determines the pooled incidence of aneurysm induction and maps the temporal progression of associated structural and hemodynamic changes. METHODS: A search of PubMed, Embase, and Web of Science (through 5 September 2026) identified experimental studies implementing the BCCAL model. We evaluated macroscopic aneurysm formation using a random-effects generalized linear mixed model (GLMM). Destructive aneurysmal remodeling, for which GLMM was not statistically appropriate due to a uniform event rate, was assessed as an exact binomial proportion. Secondary outcomes (mortality, hemodynamics, and histopathological degradation) were assessed utilizing single-arm continuous, comparative binary, and multilevel mixed-effects meta-analyses, with cluster-robust sensitivity analyses where repeated measures were present. RESULTS: Across 22 included studies, the pooled incidence of macroscopic aneurysm formation was 23.4% (k = 3 studies), while destructive structural injury was reported in all animals examined for that outcome, though its operational definition varied across studies. BCCAL increased absolute mortality risk by 16.6% compared with sham controls. Acutely (1 to 7 days), basilar blood flow velocity and WSS rose significantly, accompanying rapid internal elastic lamina (IEL) destruction (mean gap 507.34 µm) and media thinning (450.32 µm). Flow rate also increased, though this trend did not survive cluster-robust sensitivity analysis. In the chronic phase (>7 days), compensatory vasodilatation attenuated localized hemodynamic stress. Whether the structural defect subsequently remained stable or progressed further could not be conclusively determined. CONCLUSIONS: The rabbit BCCAL model reliably induces early-stage aneurysmal remodeling via a rapid mechanical insult, though its long-term structural trajectory remains unresolved. This study provides preliminary incidence and mortality estimates to help inform sample size and power calculations for future preclinical neurovascular trials.