Background and objective: Neurological dysfunction is a common problem after cardiac surgery with cardiopulmonary bypass (CPB). Cerebral ischaemia associated with the use of CPB may result in a release of neuronal–ischaemic markers and a subsequent cerebral inflammatory response which may additionally release inflammatory cytokines. In order to locate the origin and to quantify the release of neuronal–ischaemic markers and cytokines we investigated arterial–cerebral venous concentration gradients during and after CPB in a clinical setting.
Methods: In twenty-five patients scheduled for coronary artery bypass grafting surgery we measured the plasma concentration of neuron-specific enolase, S-100β protein as well as interleukins (IL) IL-6, IL-8 and IL-10 from arterial and cerebral venous blood samples prior to surgery (baseline), during hypothermic CPB at 32°C, after termination of bypass, as well as 2, 4 and 6 h after admission to the intensive care unit.
Results: Arterial–cerebral venous concentration gradients of neuron-specific enolase, S-100β, IL-6, IL-8 and IL-10 were neither detectable during nor after CPB. Compared to the baseline period, S-100β and neuron-specific enolase significantly increased during hypothermic CPB. After termination of CPB, neuronal–ischaemic markers as well as cytokines were increased and remained elevated during the investigated time course without reaching baseline values.
Conclusions: Although we found an overall increase in plasma concentrations of neuronal–ischaemic markers, IL-6, IL-8 and IL-10 during and after CPB, arterial–cerebral venous gradients were not detectable for any of these parameters. Our results suggest that the increase of investigated parameters associated with the use of CPB are not primarily caused by a cerebral inflammatory response but rather reflect a release from other sources in the systemic circulation.