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.
Highlights
Delayed cerebral vasospasm (DCVS) and delayed cerebral ischemia (DCI) are severe complications of subarachnoid hemorrhage (SAH)
IL-1 stimulates the release of IL-6 from mast cells [17], which have been described to be present in the aneurysm wall of SAH patients and the muscular layer of cerebral arteries [18,19]
We aimed to evaluate the levels of systemic and cerebrospinal fluid (CSF) IL-1α in an established extracranial intracranial closed rabbit SAH model and to analyze if there are any correlations with delayed cerebral vasospasm (DCVS)
Summary
Delayed cerebral vasospasm (DCVS) and delayed cerebral ischemia (DCI) are severe complications of subarachnoid hemorrhage (SAH). Different cytokines and interleukins have been described as mediators of the inflammation cascade initiated by blood products in the subarachnoid space, leading to DCVS and DCI [1,2,3,4]. IL-1 has been described to be a key mediator of neuronal injury after acute brain injury [15,16] It usually upregulates the expression of interleukin-6 (IL-6), which triggers local inflammation and activation of the systemic acute phase response. The inflammatory pathway in cerebrospinal fluid (CSF) leads to delayed cerebral vasospasm (DCVS) and delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH). 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. There was a significant increase of systemic
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