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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@ic.ac.uk

The first 20% of the full text of this article appears below.

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, . . . [Full Text of this Article]




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[Abstract] [Full Text] [PDF]


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