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J Thorac Cardiovasc Surg 2008;135:999-1006
© 2008 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology

The inflammatory effect of cardiopulmonary bypass on leukocyte extravasation in vivo

^a British Heart Foundation, the Cardiothoracic Surgery, Hammersmith Hospital, London, United Kingdom
^b Cardiovascular Medicine Units, Eric Bywaters Centre, Imperial College Faculty of Medicine, Hammersmith Hospital, London, United Kingdom
^c Edmund Cohen Laboratory for Vascular Research, Chronic Disease Research Centre, UWI, Bridgetown, Barbados

Received for publication March 16, 2007; revisions received August 22, 2007; accepted for publication August 30, 2007.

^_* Address for reprints: Dr. Clive Landis, Edmund Cohen Laboratory for Vascular Research, Chronic Disease Research Centre, UWI, Jemmotts Lane, Bridgetown BB 11115, Barbados (Email: clive.landis{at}uwichill.edu.bb).

Objective: Extravascular trafficking of leukocytes into organs is thought to play a major role in the pathophysiologic mechanisms of the inflammatory response to cardiopulmonary bypass, yet leukocyte extravasation is difficult to study clinically. Here we have tested the hypothesis that leukocyte emigration into skin blisters can provide a way to monitor the inflammatory effect of cardiopulmonary bypass that allows testing of anti-inflammatory interventions (exemplified by aprotinin).

Methods: Patients undergoing primary elective coronary artery bypass grafting (n = 14) were randomized into 2 equal groups to receive saline infusion during cardiopulmonary bypass (control group) or high-dose aprotinin. Experimental skin blisters (in duplicate) were induced on the forearm by means of topical application of the vesicant cantharidin, and blister fluid was sampled at 5 hours postoperatively. Inflammatory leukocyte subsets in blister fluid were analyzed by means of flow cytometry by using expression of CD11b and CD62L as a phenotypic marker of activation.

Results: In the control group of patients, cardiopulmonary bypass surgery triggered a 381% increase in leukocyte extravasation into the skin compared with reference blisters carried out before surgical intervention, with neutrophil (P = .014), monocyte (P = .014), and eosinophil (P = .009) levels all statistically significantly increased. In the aprotinin group there was no statistically significant increase during cardiopulmonary bypass surgery in any inflammatory leukocyte subset. The activation phenotype of extravascular leukocytes was not significantly altered between surgical groups.

Conclusions: This study introduces the cantharidin blister technique as a powerful new research tool for analyzing the inflammatory effect of cardiopulmonary bypass in vivo. It has provided detailed molecular insight into the extravascular leukocyte population during cardiopulmonary bypass. Although aprotinin blocked cardiopulmonary bypass–dependent extravasation of leukocytes, there was no change in their CD11b/CD62L activation status. The cantharidin skin test thus represents a novel research tool for evaluating future anti-inflammatory interventions in cardiothoracic surgery.