Surgical trauma and reperfusion injury appear to represent the predominant factors resulting in immunologic changes after cardiac surgery. Cardiopulmonary bypass (CPB) may be less important for immune response and acute-phase reactions than previously suspected. In addition, our data indicate a relationship between IL-6 synthesis and the degree of surgical trauma. IL-8 appears to be elevated only after cardiac surgery whereas PCT liberation depended on the use of ECC.

Due to the significant differences in the degree of increase, PCT appears to be useful in discriminating between acute phase response following cardiac surgery with CPB or local problems and systemic infections, with additional CRP-measurement increasing the specificity.

No abstract

Growing evidence indicates that cell-mediated immunity is altered after cardiac surgery with cardiopulmonary bypass (CPB). The objective of this prospective randomized study was to investigate (1) if an imbalance in T-helper cell (TH) subsets, i.e. TH1/TH2, may be responsible for these alterations and (2) if they can be counteracted. Twenty patients formed control group A. Twenty group B patients received indomethacin and thymopentin for immunomodulation. In vitro tests included measurements of TH, interleukin (IL)-2 as a cytokine primarily produced by TH1 cells, and IL-6 as a cytokine primarily produced by TH2. Delayed-type hypersensitivity (DTH) skin response and specific antibody (AB) production were used as in vivo tests for TH1- and TH2-induced immune response, respectively. Postoperatively, group A patients showed a persistent, significant reduction of TH, IL-2 synthesis and DTH skin response as compared to baseline values, while IL-6 synthesis remained unaltered and AB production increased (P < 0.05). In group B patients no change in TH, IL-2 and IL-6 synthesis, or DTH skin response was observed (P < 0.05 vs A). Postoperative AB production increased significantly in group B. These results indicate a significant suppression of TH1-induced cell-mediated immune response following CPB, while TH2-induced response remains normal. A normal TH2 response may be helpful for recovery following cardiac surgery by cleaning the body of the byproducts of CPB. A suppression of TH1 response may gain clinical significance whenever a postoperative infection requires this response, but can be effectively counteracted by immunomodulatory intervention with indomethacin and thymopentin.

The number of immune cells of the specific and the non-specific immune system is not reduced in the immediate postoperative period. Haemodilution thus has no detectable effect on immune function at this time point. Beginning on d1, the function of specific immune cells, especially TH lymphocytes, is severely suppressed. This functional alteration appears not to be preceded by T cell activation during CPB. Although TH cell activity begins to increase on d1, cytokine synthesis is reduced. When cytokine synthesis is corrected to the absolute number of TH cells in culture, there is strong evidence for an increase in TH2 cell activity. On the whole, these results corroborate the hypothesis of a TH1/TH2 shift that is primarily caused by an alteration of TH1 function. Neither haemodilution nor a preceding activation plays a major role.