In the subarachnoid hemorrhage (SAH) blood mixes with cerebrospinal fluid, what starts immunoinflammatory
processes - increased synthesis of proinflammatory cytokines, and formation of reactive oxygen species
(ROS), resulting in pre-activation of different populations of peripheral leukocytes. Migration of leukocytes to the brain
parenchyma through broken blood brain barrier may produce extra brain tissue injury besides of that resulting from SAH.
We examined in adult rats the effect of interleukin-1β (IL-1β) neutralization on secretion of cytokines as well as
production of ROS in the course of SAH.
SAH was produced by injection of 150 μL of autologous arterial blood into cisterna magna. In 50% of animals, IL-1beta
activity was inhibited by intracerebroventricular administration of anti-rat IL-1β antibodies. Ninety minutes or 24 hrs
following surgery, blood samples were drawn from the extraorbital plexus and centrifuged to obtain two leukocyte
subpopulations – polymorphonuclear (PMN) and mononuclear (MN). The chemiluminescence, a hallmark of ROS
synthesis, was measured in PMNs. In supernatants from MNs cultures, concentrations endothelin-1 (ET-1), tumor
necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were assessed.
SAH caused the increase ofn PMNs chemiluminescence as well as the increase of production of ET-1 and TNF-α by MNs
but had no influence on IL-6 concentration. Neutralization of IL-1β resulted in significant decrease of chemiluminescence
as well as concentration of both ET-1 and TNF-α, while IL-6 concentration was increased.
These revealed an important role of IL-1β in the activation of peripheral leukocytes in the course of subarachnoid