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Ann Thorac Surg 1999;67:596
© 1999 The Society of Thoracic Surgeons
a Cardiovascular Surgery Discipline, Escola Paulista de Medicina, Federal University of São Paulo, Rua Botucatu 740, São Paulo 04023-900, Brazil
We appreciate the interest and comments of Dr Markewitz on our work. However, we feel that he failed to understand the real scope of our results and conclusions.
First, this was a unique model of cardiopulmonary bypass (CPB)induced tumor necrosis factor (TNF)-
release because we have studied the same disease (coronary artery disease) in patients who underwent the same procedure (coronary artery bypass grafting) and differed only with regard to the use of CPB circuit. Former studies have compared bypass grafting with other noncardiac surgical procedures.
Tumor necrosis factor-
was detected in 6 of 10 patients undergoing bypass grafting with CPB and in none without CPB. The difference was statistically significant and points out that the former patients were exposed to inflammatory stimulus not present in the latter ones. A recent study from Germany has just confirmed these findings [1]. Lack of detection in 4 of 10 patients is not surprising and may be due to insufficient blood samples collected for testing as well as the presence of levels below the limit of assay detection. Moreover, even in patients with sepsis most previous reports did not document detection of TNF-
in 100% of patients.
The suggestion that TNF-
may be related to the adverse effects seen in patients with CPB was based on the described biologic effects of this cytokine and its pivotal role in the inflammatory response. This was not a demonstration of causeeffect phenomena but a suggestion that we believe can be derived from our data. More convincing data about the role of TNF-
in these alterations could be generated if this cytokine, along with other inflammatory mediators, was blocked in patients undergoing bypass grafting with CPB. We have conducted a prospective, randomized trial in such patients that adds evidence of a casual effect (unpublished data).
We are aware of the lack of efficacy of TNF-
blockage in sepsis. However, we assume some differences in both models of inflammatory response. In sepsis a dual role for TNF-
has been demonstrated because there is a replicating microorganism to be destroyed. During CPB, an inflammatory response is initiated by contact with foreign surfaces and possible contamination by endotoxins. In such cases, the harmful effects of TNF-
may exceed its benefit for host defense.
Although many more questions about the inflammatory response after CPB need to be answered, our work did provide a new contribution to this field.
References
Related Article
and cardiac surgical procedures: still more questions than answers
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