OBJECTIVES To observe glymphatic transport and evaluate enlarged perivascular spaces (PVSs) in spontaneously hypertensive rats (SHRs). METHODS SHRs were used as an animal model of cerebral small vessel disease, and Wistar Kyoto (WKY) rats were used as the control group. Histopathology was used to evaluate the enlargement of PVSs. A fluorescent tracer was infused into the cisterna magna of rats, and the proportion of the brain parenchyma area exposed to the fluorescent tracer was later quantified to evaluate the influx and efflux function of the glymphatic system. The global and polarized expression of aquaporin protein 4 (AQP4) was analyzed by immunofluorescence. RESULTS Compared with WKY rats, SHRs exhibited obviously enlarged PVSs and significantly decreased influx and efflux function of the glymphatic system. The results showed a significant decrease in AQP4 polarity in SHRs, but a difference in global AQP4 expression was not observed between SHRs and WKY rats. CONCLUSIONS Impaired glymphatic transport may be involved in the pathogenesis of arteriolosclerotic cerebral small vessel disease, and enlarged PVSs may be a manifestation of the impaired glymphatic system.

中文翻译：

---

在脑小血管疾病的动物模型中伴随血管周围空间的扩大和淋巴管转运的减少。

目的 观察自发性高血压大鼠 (SHR) 的淋巴管转运并评估扩大的血管周围间隙 (PVS)。方法以SHRs作为脑小血管病动物模型，WistarKyoto(WKY)大鼠作为对照组。组织病理学用于评估 PVS 的扩大。将荧光示踪剂注入大鼠的大池，随后量化暴露于荧光示踪剂的脑实质区域的比例，以评估淋巴系统的流入和流出功能。通过免疫荧光分析水通道蛋白 4 (AQP4) 的全局和极化表达。结果与WKY大鼠相比，SHRs的PVSs明显增大，glymphatic系统的流入流出功能明显降低。结果显示 SHR 中 AQP4 极性显着降低，但 SHR 和 WKY 大鼠之间未观察到整体 AQP4 表达的差异。结论 血管硬化性脑小血管病的发病机制可能涉及glymphatic运输受损，PVS扩大可能是glymphatic系统受损的表现。