J Neurol Surg A Cent Eur Neurosurg 2015; 76 - A005
DOI: 10.1055/s-0035-1564498

The Role of IL-6, ET-1 in the Pathophysiology of Vasospasm, Delayed Cerebral Injury after Subarachnoid Hemorrhage

D. Croci 1, 2, E. Nevzati 1, 2, T. Hornemann 3, D. Hiroki 1, 2, S. Schöpf 1, 2, D. Coluccia 1, 2, J. Fandino 1, 2, S. Marbacher 1, 2, C. Muroi 1, 2
  • 1NEURO Lab, Research Group for Experimental Neurosurgery and Neurocritical Care, Department of Intensive Care Medicine, University Hospital and University of Bern, Bern, Switzerland
  • 2Department of Neurosurgery, Kantonsspital Aarau, Aarau, Switzerland
  • 3University Hospital Zurich, Institute for Clinical Chemistry, Zurich, Switzerland

Aim: Cerebrovascular vasospasm (CVS) is the most common complication of subarachnoid hemorrhage (SAH). Seventy percent of SAH patients present radiological sign of CVS and 30% are symptomatic. Despite progress in the treatment of SAH and CVS, the neurological outcome of affected patients remains poor. The inflammatory pathway due to blood hemolysis in cerebrospinal fluid (CSF) is one of the causes leading to CVS and delayed cerebral injury (DCI). Animal and human studies demonstrated that increased CSF levels of IL-6 and ET-1 after SAH correspond to CVS and worse outcome. The aim was to study the pathophysiological relationship between IL-6 and ET-1 in a closed cranium acute SAH model in the rabbit. Methods: Twenty-four New Zealand white rabbits were randomized in three different groups: (1) SAH group (n = 10); (2) IL-6 injection group (n = 10); and (3) sham-operated group (n = 4). In the first group, SAH was induced by extracranial‒intracranial shunting from the subclavian artery into the cerebral cistern. In the second group, IL-6 was injected directly into the cisterna magna. The sham-operated group served as control. Digital subtraction angiography (DSA) to measure the diameter of the basilar artery of rabbits, CSF, and blood samples were performed at day 0 previous to intervention and at follow-up, at day 3 postintervention. The amount of IL-6, ET-1 in plasma and CSF were measured with ELISA. Results: A significant increases between baseline (day 0) and follow-up (day 3) of IL-6 in CSF could be found in the SAH and IL-6 group. A significant correlation between IL-6 and ET-1 levels could be found in CSF was found (Pearson's r = 0.454, p = 0.003). On DSA, a trend of developing CVS in the SAH with relative CVS of 26.0% (SD +/− 20.4%) and 16.7% (SD +/ − 15.0%) in IL-6 group compared with 9.4% (SD +/ − 5.5%) in the sham group was found. Conclusions: This study shows that IL-6 is involved in the development of CVS. Furthermore, the results indicate that there is a correlation between IL-6 and ET-1 in the pathophysiology of CVS. Further in-vivo studies are warranted to better elucidate the role of IL-6 in stimulating ET-1 leading to CVS after SAH.