Development of an Acute Intracranial Hypertension-Induced Rat Model for Terson Syndrome and Mechanisms of...

This study aimed to establish an experimental rat model of Terson syndrome and explore occludin's role in blood-retinal barrier disruption.

We induced acute intracranial pressure elevation in rats via cisterna magna normal saline or autologous blood injections (0.25-0.75 mL over 30-60 s) and monitored intraocular hemorrhage over 7 days. Retinal leakage was assessed via fluorescein flat-mounts, vascular endothelial growth factor (VEGF) and interleukin-6 (IL-6) via enzyme-linked immunosorbent assay (ELISA), and occludin via immunofluorescence.

Both injections into the cisterna magna effectively induced Terson syndrome manifestations. All experimental groups demonstrated significant fluorescein leakage from posterior pole vessels within 1 min post-injection, with predominant extravasation observed along superficial retinal veins. While venous leakage progressively diminished after 30 min, peripheral capillary leakage emerged. Retinal VEGF levels significantly increased at 30 and 60 min post-intracranial pressure elevation, while IL-6 levels rose at 30 min. Quantitative analysis demonstrated no significant alterations in total retinal occludin levels. Additionally, stratified analysis revealed unchanged occludin levels in both the intermediate capillary plexus (ICP) and the deep capillary plexus (DCP). The superficial vascular complex (SVC) exhibited significant occludin reduction at 1, 30, and 60 min post-induction and the retinal pigment epithelium (RPE) showed delayed occludin downregulation at day 5.

This study established a preliminary experimental rat model of Terson syndrome. The model suggests Terson syndrome results from intracranial hypertension compressing the central retinal vein, disrupting tight junctions, and causing blood-retinal barrier failure, leading to hemorrhage.