Abstract
Abundant erythrocytes remain and lyse partially in the subarachnoid space after severe subarachnoid haemorrhage (SAH). But the effect of subarachnoid erythrocyte lysate on brain injury is still not completely clear. In this study, autologous erythrocytes (the non-lysate group) and their lysate (the lysate group) were injected separately into the cistern magna of rabbits to induce a model of experimental SAH, although the control group received isotonic sodium chloride solution instead of erythrocyte solution. Results showed that vasospasm of the basilar artery was observed at 72h after experimental SAH, but there was no significant difference between the non-lysate group and the lysate group. Brain injury was more severe in the lysate group than in the non-lysate group. Meanwhile, the levels of peroxiredoxin 2 (Prx2), IL-6 and TNF-α in brain cortex and in CSF were significantly higher in the lysate group than those in the non-lysate group. These results demonstrated that brain injury was more likely to be caused by erythrocyte lysate than by intact erythrocytes in subarachnoid space, and inflammation response positively correlated with Prx2 expression might be involved in mechanism of brain injury after SAH.
Highlights
There were several common methods to induce an animal model of experimental subarachnoid haemorrhage (SAH), such as autologous blood injection into cisterna magna [1] or prechiasmatic cistern [2], endovascular perforation [3]
Studies mainly focused on cerebral vasospasm (CVS), and recent studies were more inclined to early brain injury (EBI)
Previous studies showed that brain injury was observed when the whole blood lysate was injected into the brain cortex of mice [4] or cisterna magna of rabbits [5], vasospasm of the basilar artery was existed when the whole blood lysate was injected into cisterna magna of canine [6]
Summary
There were several common methods to induce an animal model of experimental subarachnoid haemorrhage (SAH), such as autologous blood injection into cisterna magna [1] or prechiasmatic cistern [2], endovascular perforation [3]. The mechanisms of brain damage after SAH were very complex and not yet fully understood. Studies mainly focused on cerebral vasospasm (CVS), and recent studies were more inclined to early brain injury (EBI). No matter what kind of study, the damage factor chosen was usually the whole blood or its lysate. Even though aneurysms had been treated, abundant erythrocytes and its lysate in the form of blood clots or free in the cerebrospinal fluid (CSF) still remained in the subarachnoid space, and was hard to be cleared in a short time. It was extremely important to understand the role of subarachnoid erythrocytes and their lysate on CVS or on brain injury. The roles of subarachnoid erythrocytes and their lysate on brain injury are still not absolutely understood
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