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Ann Thorac Surg 2003;75:215-216
© 2003 The Society of Thoracic Surgeons

Invited commentary

Terrance Gourlay, PhDa, George Asimakopoulos, MDa

a Hammersmith Hospital, Department of Cardiac Surgery, Imperial College Faculty of Medicine, Hammersmith Hospital, DuCane Road, London W12 0NN, UK

e-mail: tgourlay{at}ic.ac.uk

We congratulte the authors on carrying out a very well-designed study. The authors employed two discreet methods for activating inflammatory processes: thrombin stimulation and haemorrhage/reperfusion.

There is a body of evidence that proposes that aprotinin affects thrombosis stimulated inflammatory processes through its action on protease-activated receptor (PAR-1) and -4. Pullis and associates [1] have shown that aprotinin prevents proteolysis on PAR-1, which is the major thrombosis receptor on platelets. The authors further speculate that aprotinin should also affect proteolytic cleavage on PAR-1, which is present on both leukocytes and endothelium. In a recent series of studies, Vergnolle and associates [2] thrombosis was shown to be responsible for leukocyte rolling and adhesion to rat mesentery. We were somewhat surprised that the works of Poullis and Vergnolle were not referred to by Pruefer and associates.

The hemorrhagic model of the inflammatory response described by the authors involves a mode of neutrophil–endothelial interaction which resembles the phenomena, that takes place during ischaemia–reperfusion injury wherein previously ischaemic tissues secrete chemo attractant factors such as interleukin-8 or PAF, which activate neutrophils. This model is similar to one used and reported by our group [3] and referred to by the authors. Neutrophil–endothelial cell interactions within the first 120 minutes of inflammatory response are likely to be affected by P-selectin as stated by Pruefer and associates, but also by L-selectin expression. Aprotinin was shown to affect L-selectin shedding on neutrophils by our own group [4], although the physiological significance of this process in not as yet entirely understood.

Aprotinin has been shown to have many beneficial effects in clinical practice, although the precise mechanisms through which these benefits are achieved are not fully understood. These remain the target of considerable research effort, and the authors of this paper are to be congratulated for tackling such a complex issue from two interesting perspectives.

References

  1. Poullis M., Manning R., Laffan M., Haskard D.O., Taylor K.M., Landis R.C. The antithrombotic effect of aprotinin: actions mediated via the protease activated receptor. J Thorac Cardiovasc Surg 2000;120:370-378.[Abstract/Free Full Text]
  2. Vergnolle N., Derian C.K., D’Andrea M.R., Steinhoff M., Andrade-Gordon P. Characterization of thrombin-induced leukocyte rolling and adherence: a potential proinflammatory role for proteinase-activated receptor-4. J Immunol 2002;169:1467-1473.[Abstract/Free Full Text]
  3. Asimakopoulos G., Thompson R., Nourshargh S. An anti-inflammatory property of aprotinin detected at the level of leukocyte extravasation. J Thorac Cardiovasc Surg 2000;120:361-369.[Abstract/Free Full Text]
  4. Asimakopoulos G., Taylor K.M., Haskard D.O., Landis R.C. Inhibition of neutrophil L-selectin shedding: a potential anti-inflammatory effect of aprotinin. Perfusion 2000;15:495-499.[Abstract/Free Full Text]



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[Abstract] [Full Text] [PDF]

This Article
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