Systemic and CSF Interleukin-1α Expression in a Rabbit Closed Cranium Subarachnoid Hemorrhage Model: An Exploratory Study

Abstract

Background: The inflammatory pathway in cerebrospinal fluid (CSF) leads to delayed cerebral vasospasm (DCVS) and delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH). The role of IL-1α has never been evaluated in a rabbit SAH model. The aim of our study is to analyze systemic and CSF changes of IL-1α, and to evaluate potential associations with the onset of DCVS in a rabbit closed cranium SAH model. Methods: 17 New Zealand white rabbits were randomized into two groups, SAH (n = 12) and sham (n = 5). In the first group, SAH was induced by extracranial-intracranial shunting from the subclavian artery into the cerebral cistern of magna under intracranial pressure (ICP) monitoring. The sham group served as a control. The CSF and blood samples for IL-1α measurement were taken at day zero before SAH induction and at day three. Results: There was a significant increase of ICP (p = 0.00009) and a decrease of cerebral perfusion pressure (CPP) (p = 0.00089) during SAH induction. At follow up, there was a significant increase of systemic IL-1α in the SAH as compared with the sham group (p = 0.042). There was no statistically significant difference in the CSF values in both groups. The CSF IL-1α values showed a correlation trend of DCVS. Conclusions: Systemic IL-1α levels are elevated after SAH induction in a rabbit SAH model.

Clinical Studies and Pre-clinical Animal Models on Facial Nerve Preservation, Reconstruction, and Regeneration Following Cerebellopontine Angle Tumor Surgery–A Systematic Review and Future Perspectives

“…Additionally, access to the CSF system in rabbits is easily given by applying a puncture needle directly into the cisterna magna. Techniques for this approach have been described elsewhere (Croci et al, 2019 ). With a fixing system, as well with implantation of a subcutaneous minipump, a continuous and dose dependent application of medication, even neural growth factors, might be feasible (Croci et al, 2019 ).…”

Levosimendan as a therapeutic strategy to prevent neuroinflammation after aneurysmal subarachnoid hemorrhage?

“…4 Endothelin-1 (ET-1) triggers DCVS by targeting the ET-A receptor (ET A-R ), considering the established inactivation of the vasorelaxant ET-B 1 receptors (ET B1-R ) post-SAH. 1 Driving factors for cerebral inflammation (CI), contributing to DCVS and neurodegeneration as well, include peripheral immune cells, 5 inflammatory cytokines, 6 serotonin (5-HT), and prostaglandin F2alpha (PGF2a). 7 Levosimendan (LV), a calcium channel sensitizer, is already a mainstay in the treatment of congestive heart failure, as well as after SAH in patients suffering from DCVS and/or stress cardiomyopathy.…”

“… 4 Endothelin-1 (ET-1) triggers DCVS by targeting the ET-A receptor (ET A-R ), considering the established inactivation of the vasorelaxant ET-B 1 receptors (ET B1-R ) post-SAH. 1 Driving factors for cerebral inflammation (CI), contributing to DCVS and neurodegeneration as well, include peripheral immune cells, 5 inflammatory cytokines, 6 serotonin (5-HT), and prostaglandin F2alpha (PGF2a). 7 …”

Experimental and Clinical Treatment of Subarachnoid Hemorrhage after the Rupture of Saccular Intracranial Aneurysms

“…The call for papers on this topic was met with a great response by researchers and clinicians from all over the world. Among 16 basic science and clinical research submissions, our editorial team selected nine articles for publication after extensive peer review, which included three original papers [ 1 , 2 , 3 ], three reviews [ 4 , 5 , 6 ], two case reports [ 7 , 8 ] and one technical note [ 9 ]. The remaining seven papers were not included, thus yielding a 44% rejection rate.…”