Dexamethasone effect on sFas/sFas ligand following cardiopulmonary bypass
© The Author(s) 2001
Received: 15 January 2001
Published: 2 March 2001
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.
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.
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.