Dexamethasone effect on sFas/sFas ligand following cardiopulmonary bypass

Introduction

Steroids decrease systemic inflammation following cardiopulmonary bypass (CPB). Membrane bound Fas is a receptor found on many cells, which stimulates apoptosis when cleaved by Fas ligand (FasL). FasL also has a proinflammatory role and is released following ischaemia-reperfusion. We wished to investigate the time course of release of the soluble forms of Fas and FasL (sFas, sFasL) post CPB, and whether steroid pre-treatment altered the response.

Method

Twenty-seven children with congenital heart disease were studied, median (IQ) age 7 (0.4-10) months. Patients were given 0.25 mg/kg dexamethasone (DEX) (n = 13) or no DEX (n = 14) at induction of anaesthesia. Groups were well matched in terms of age, type of operation, length of CPB, cross clamp, and circulatory arrest (all P > 0.15). sFas, sFasL and interleukin (IL) 6 (a marker of cytokine response) were measured over 24 hours by double sandwich ELISA.

Results

DEX significantly blunted the release of IL6 and sFas, but not sFasL. The DEX group exhibited a decreased clinical inflammatory response post CPB as evidenced by a lower temperature, less colloid requirement, chest drain loss, acidosis, hyperlactataemia and coagulopathy (all P < 0.05).

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Conclusion

DEX blunts IL6 and sFas but not sFasL release following CPB, attenuating clinical inflammatory response. The significance of the sFas response is unclear; this may be a passive marker of a decreased inflammatory response but decreased levels may also negatively influence apoptosis/inflammation by being less able to 'mop-up' excess membrane and soluble FasL.