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CARDIOVASCULAR
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Volume 6, 2001, No 1 |
Temperature
and Inflammatory Response on Cardiopulmonary Bypass
A. Bel, N. Elleuch, E.
Florens, P. Menasché
Cardiopulmonary
bypass (CPB) can substantially contribute to organ dysfunction, and in
particular lung, with subsequent morbidity and to peripheral vasodilatation,
with the need of vasopressor agents, potentially deleterious for some organ
perfusions or newly constructed bypass grafts. These clinical concerns are
related to an induced inflammatory response, involving both humoral and cellular
mediators. Among the former, the complement system is assumed to play a major
role, although not exclusive, whereas neutrophils account for most of the
cell-mediated inflammatory tissue damage. Theoretically, the systemic
temperature during CPB may influence the magnitude of these inflammatory
responses.
It has been demonstrated that maintenance of normothermia during bypass may
increase the extent of the inflammatory response to CPB over that seen under
hypothermic conditions. In these latter conditions, the inflammatory mediators
are also activated, but the peak levels are often delayed beyond the end of CPB.
In an attempt to minimize the systemic inflammatory response to bypass and the
subsequent post-perfusion syndrome, the concept of tepid CPB and cardioplegia
has been developed.
(CVE. 2001; 6 (1): 25-28)
Key words: cardiopulmonary bypass, temperature, inflammation, complement, cytokines
Alain
Bel, M.D.
Department of Cardiovascular Surgery
Hôpital Bichat
46 rue Henri Huchard
F-75877 Paris Cedex 18
France
PABST SCIENCE PUBLISHERS
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