Regulation of acute phase response after cardiopulmonary bypass by immunomodulation

The object of this prospective, randomized trial was to study the dysregulation effects of cardiopulmonary bypass on the synthesis pattern of interleukin-1, tumor necrosis factor, and interleukin-6, which have been identified as the key mediators of acute phase response. In addition, the counterregu...

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Veröffentlicht in:The Annals of thoracic surgery 1993-02, Vol.55 (2), p.389-394
Hauptverfasser: Markewitz, Andreas, Faist, Eugen, Lang, Stephan, Endres, Stefan, Hültner, Lothar, Reichart, Bruno
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Sprache:eng
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Zusammenfassung:The object of this prospective, randomized trial was to study the dysregulation effects of cardiopulmonary bypass on the synthesis pattern of interleukin-1, tumor necrosis factor, and interleukin-6, which have been identified as the key mediators of acute phase response. In addition, the counterregulation achieved by administration of indomethacin, which blocks the downregulating mediator prostaglandin E 2, or indomethacin combined with thymopentin, which enhances T-lymphocytic reactivity, was investigated. Sixty patients who had undergone open heart operations were included in the study. These patients were divided into three groups: group A (n = 20) received intravenous indomethacin alone, group B (n = 20) received both indomethacin and thymopentin, and group C (n = 20) served as control. In control patients interleukin-1 and tumor necrosis factor synthesis were suppressed postoperatively. This effect was significantly counteracted by indomethacin with no further improvement by adding thymopentin. Interleukin-6 synthesis increased in all groups. Although indomethacin treatment alone had little effect on this phenomenon, additional administration of thymopentin significantly reduced elevated interleukin-6 synthesis. Corresponding differences in clinical outcome could not be detected due to small patient numbers. This study was, however, able to demonstrate that an immunomodulatory therapy can influence alterations in immune mechanisms after cardiopulmonary bypass.
ISSN:0003-4975
1552-6259
DOI:10.1016/0003-4975(93)91007-A