establishment-rat-model-superior-sagittal-sinus-occlusion-via-thread

Establishment of a Rat Model of Superior Sagittal-Sinus Occlusion via a Thread-Embolism Method

The mechanisms contributing to the natural onset of cerebral venous sinus thrombosis (CVST) are mostly unknown, and a variety of uncontrollable factors ...

the Hospital of Changle

There are many uncontrollable factors in the pathogenesis of cerebral venous sinus thrombosis (CVST). In order to further explore the pathophysiology and morphology of CVST, it is necessary to establish a highly compatible CVST animal model that can standardize the site and stage of venous thrombosis. The present study employed the insertion of a self-made thread embolism into the superior sagittal sinus (SSS) to establish a rat model of SSS occlusion that emulates CVST. The thread embolism was removed after 6 h of SSS occlusion in order to achieve recanalization. After successful preparation of the model, the cerebral blood flow (CBF) status and ultrastructural changes of the blood-brain barrier (BBB) were monitored. This CVST model was able to achieve continuously high occlusion of SSS. The parasagittal venous-collateral circulation underwent extensive compensation and recombination, which alleviated blood flow stasis and brain tissue hypoxia caused by restricted reflux. Removing SSS occlusion significantly improved cerebral circulation, reduced brain edema, and accelerated the receding of brain edema. This study established a new model of acute occlusion and recanalization of SSS in rats via a thread-embolism method, which standardized the ischemic site and stage of venous thrombosis. In addition, our study suggests that promoting collateral circulation may be a potential treatment for promoting brain protection.

Establishment of a Rat Model of Superior Sagittal-Sinus Occlusion and Recanalization via a Thread-Embolism Method.

Mass evacuation with decompressive craniotomy is considered a standard intervention for acute subdural hematoma (ASDH). However, hemispheric swelling complicates the intraoperative and postoperative management of ASDH patients, and previous studies have revealed that this approach can damage ischemic/reperfusion (I/R) injury. Few studies have focused on the cerebrovascular response following traumatic brain injury (TBI). To characterize the relative cerebral blood flow (rCBF) before and after removal of the hematoma, rats were injured by a subdural infusion of 400 μL of venous blood or paraffin oil. MRI scans were performed. Then, we monitored cortical rCBF during hematoma removal in real time using laser speckle imaging (LSCI) in ASDH rats. The CBF of arteriovenous and capillary regions were quantified and normalized to their own baseline values via a custom algorithm. In the sham group, the cortical CBF was higher post-craniotomy than pre-craniotomy. However, in the hematoma injection group, the CBF of arteries and capillaries was higher while the venous CBF was lower post-craniotomy than pre-craniotomy. The difference in the changes in vein CBF that occurred between the two groups was statistically significant. The three components of the vascular system showed heterogeneous responses to craniotomy, which may be the basis for secondary brain injury.

Weiming Xu

Department of Neurosurgery

the Hospital of Changle

Establishment of a Rat Model of Superior Sagittal-Sinus Occlusion via a Thread-Embolism Method