Corticosteroids reduce neuron-specific-enolase liberation after cardiopulmonary bypass in men

Introduction

Cardiopulmonary bypass (CPB) is associated with a significant morbidity due to central nervous system dysfunction [1]. Part of this damage may be related to the inflammatory response generated by CPB [2]. Neuron-specific enolase (NSE) is a neuron-specific enzyme that is liberated during brain injury and has recently been proposed as a marker of cerebral ischemia after CPB [3]. Because corticosteroids significantly reduce the inflammatory reaction to CPB [4], we investigated whether pretreatment with corticosteroids can influence the liberation of NSE during CPB.

Materials and method

After institutional approval, 45 patients scheduled for nonemergency coronary artery bypass grafting (CABG) with CPB were divided into four groups: the control group (CTRL; n = 17) received no corticosteroids; the DXM group (n = 7) received 2 mg/kg dexamethasone; and the MPS10 group (n = 14) received 10 mg/kg and the MPS30 (n = 7) group received 30 mg/kg methylprednisolone intravenously 2 h before surgery. CPB was conducted under moderate hypothermia (29-30 °C) using a cold crystalloid cardioplegia and a nonpulsatile flow. Anaesthesia consisted of a continuous infusion of sufentanil, midazolam and pancuronium. No aprotinin was used. We measured NSE levels before induction of anaesthesia and 4 h after CPB. For each patient we calculated the change in NSE concentration as follows: NSE (at 4 h)-NSE (baseline). We also measured tumor necrosis factor (TNF) and interleukin (IL)-8 at the same time. There were no differences between the groups regarding age, duration of CPB, aortic cross-clamping time or number of grafts.

Results and discussion

The CTRL group showed a significant increase in NSE after CPB, whereas in all three corticosteroid groups NSE was significantly lower (Fig. 1).

TNF and IL-8 liberation were significantly and equally reduced in all three treatment groups. This suppression of the inflammatory response might lead to less neutrophil adhesion and migration, resulting in less tissue damage by proteolytic enzymes and oxygen-free radicals.

Figure 1

Neuron-specific enolase (NSE) levels. The control group (CTRL; n = 17) received no corticosteroids; the DXM group (n = 7) received 2 mg/kg dexamethasone; and the MPS10 group (n = 14) received 10 mg/kg and the MPS30 (n = 7) group received 30 mg/kg methylprednisolone intravenously 2 h before surgery. ^* P < 0.05 versus CTRL group, by Mann-Whitney U-test.

Conclusion

Corticosteroids, even at moderate doses, are able to reduce the amount of NSE liberation during CPB. This may indicate less brain injury during CPB. Whether this reduction in NSE liberation translates into improved neurological outcome remains to be studied.