Volume 5 Supplement 1

21st International Symposium on Intensive Care and Emergency Medicine

Open Access

Dexamethasone effect on sFas/sFas ligand following cardiopulmonary bypass

  • U Joashi1,
  • SM Tibby1,
  • A Mayer1,
  • A Durward1,
  • C Turner1 and
  • IA Murdoch1
Critical Care20015(Suppl 1):P075


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 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).



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.

Authors’ Affiliations

Department of Paediatric Intensive Care, Guy's Hospital


© The Author(s) 2001