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European Journal of Cardio-Thoracic Surgery, Vol 7, 563-573, Copyright © 1993 by European Association for Cardio-thoracic Surgery
NE Moat, DF Shore and TW Evans
Cardiopulmonary bypass-induced organ dysfunction remains a clinical problem
in certain groups of patients. Although the pathogenesis is multifactorial,
it is likely that a panendothelial injury consequent upon widespread
humoral and cellular activation is a major contributor to this process. The
biologically active products of complement activation are certainly capable
of inducing many of the features of the post-perfusion syndrome. The
complex interactions between complement and many of the other proposed
mediators of this response also supports this contention. However, it is
equally certain that many of the other proposed mediators have some role to
play. Inhibition of one cell type or inflammatory cascade is therefore
unlikely to abolish all the adverse effects of CPB but will, at least in
experimental systems, permit a more precise determination of the
pathogenesis of this problem. The temptation to simply measure elevated
circulating levels of newly identified mediators must be resisted and more
effort applied to examining the pathophysiological effects of specific
inhibitors. This type of investigation should initially be effected in
experimental models where reproducible conditions can be ensured. In
conjunction with this, far more precise end-points are required in order to
assess the effect of any potential therapeutic intervention in a clinical
setting. In particular, new techniques of evaluating endothelial injury
need to be developed. In clinical studies careful consideration must be
given to the patient population studied. Whilst patients undergoing routine
coronary artery surgery form a relatively homogeneous group, the magnitude
of endothelial injury sustained is probably small and, especially in terms
of lung function, the signal will be diluted by other non-bypass-related
events. The study of high risk groups would seem more appropriate despite
their heterogeneity. An important unanswered question is why certain
sub-populations of patients are at increased risk of clinically relevant
bypass-induced injury. The endothelium of these patients may be different:
the neonatal pulmonary microcirculation is not the same as that of an adult
(with increased fluid filtration pressure and a higher microvascular
surface area per unit lung mass [5,6]), children with pulmonary
hypertension have histological evidence of an altered/damaged endothelium
(S.G. Haworth, Personal Communication) whilst pre-existing sepsis could
clearly induce a degree of endothelial dysfunction. A further possibility
is that the inflammatory response in these patients is already "primed".
Some patients with heart failure have been shown to have elevated
circulating TNF.(ABSTRACT TRUNCATED AT 400 WORDS)
ARTICLES
Organ dysfunction and cardiopulmonary bypass: the role of complement and complement regulatory proteins
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