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J Thorac Cardiovasc Surg 2002;123:137-144
© 2002 The American Association for Thoracic Surgery

Surgery for Congential Heart Disease

Soluble Fas may be a proinflammatory marker after cardiopulmonary bypass in children

From the Departments of Pediatric Intensive Care^a and Pediatric Cardiothoracic Surgery,^b Guy's Hospital, London, United Kingdom.

Received for publication May 11, 2001. Revisions requested June 15, 2001; revisions received July 3, 2001. Accepted for publication July 10, 2001. Address for reprints: Shane Tibby, MRCP, Department of Pediatric Intensive Care, Guy's Hospital, Saint Thomas Street, London SE1 9RT, United Kingdom (E-mail: Shane.Tibby{at}gstt.sthames.nhs.uk).

Abstract

Objectives: Ischemia-reperfusion injury after cardiopulmonary bypass is known to provoke an inflammatory response, which can be attenuated with steroid pretreatment. Cardiopulmonary bypass is also known to stimulate apoptosis. Induction of the cellular apoptotic cascade occurs via interaction between two membrane receptors: Fas and Fas ligand. Both molecules also exist in soluble forms, whose significance remains undetermined; however, both may have a proinflammatory role. We aimed to document the temporal profile of soluble Fas and soluble Fas ligand after cardiopulmonary bypass and to investigate whether steroid pretreatment alters this response.
Methods: The study was of a nonrandomized, nonblinded, prospective nature. Twenty-seven infants were monitored prospectively, of whom 13 received dexamethasone at induction of anesthesia. Soluble Fas, soluble Fas ligand, and interleukin 6 were measured from induction of anesthesia until 24 hours after admission to the intensive care unit. Data on clinical and laboratory variables were also collected at the same time intervals.
Results: As expected, dexamethasone pretreatment attenuated interleukin 6 release and the clinical systemic inflammatory response after bypass. Soluble Fas showed a remarkably similar profile to interleukin 6, in terms of temporal release and attenuation with steroids. There was also a correlation between maximum soluble Fas and markers of capillary leak (colloid requirement and drain loss). Conversely, soluble Fas ligand release was unchanged by cardiopulmonary bypass and steroid administration. However, patients with higher soluble Fas ligand levels exhibited a more dramatic drop and delayed recovery in monocyte count, consistent with the role of this molecule in apoptosis.
Conclusions: Release of soluble Fas and soluble Fas ligand follows a markedly different temporal profile after cardiopulmonary bypass. The similarity between soluble Fas and interleukin 6, together with the attenuation of both with steroids, may suggest a role for soluble Fas as a proinflammatory marker.

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