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Department of Anesthesia, Royal Victoria Hospital, Belfast, Northern Ireland Department of Microbiology and Immunobiology, Queen’s University, Belfast, Northern Ireland
To the Editor:
Harmon et al. (1) showed that clomethiazole in an isolated cardiopulmonary bypass (CPB) system (n = 5) significantly reduced IL-8, TNF-
, and IL-6. Neutrophil CD18 did not increase in either control or clomethiazole circuits, but after 120 min was lower with clomethiazole. The authors suggest that expression of CD18 reflects the whole family of ß2 integrins. This was not our experience. In a similar system (n = 10) CD18 did not increase significantly but CD11b did (2). Therefore, CD11b is a particularly useful marker in determining neutrophil inflammatory responses during isolated CPB. Although this CD11b response is consistent with the in vivo response (3), we still recommend caution when extrapolating from in vitro to in vivo. For example, methylprednisolone-mediated reduction in neutrophil CD11b expression observed at in vivo CPB (4) was not repeated in isolated CPB (2), even though methylprednisolone reduced plasma IL-8 in the isolated circuit (2).
Drugs may exert antiinflammatory effects by several mechanisms that may require a functioning antiinflammatory response.
Isolated CPB cannot generate a plasma antiinflammatory cytokine response (2,3,5). Accordingly, this system only identifies a test drug’s ability to directly reduce the proinflammatory response independent of the antiinflammatory response. This limitation needs to be considered in interpreting the results of Harmon et al. with clomethiazole.
References
, and neutrophil adhesion molecule expression during experimental extracorporeal circulation. Anesth Analg 2003; 97: 13–8.
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