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Institut de Myologie - INSERM U582, Groupe Hospitalier Pitié-Salpêtrière, 47, Boulevard de l’Hôpital, Paris 75651 Cedex 13, France
(Email: y.fromes{at}myologie.chups.jussieu.fr).
Cardiopulmonary bypass (CPB) has improved a great deal since its early applications; however, a postperfusion syndrome, mainly translated as an acute respiratory distress syndrome, still occurs in some patients. Basically, the inflammatory response to extracorporeal circulation seems to be responsible for impairment of lung function. Blood contact with nonendothelial cell surfaces in the perfusion circuit and the wound activates plasma proteins and cellular blood elements.
All surgery triggers an acute inflammatory response, but persistent exposure of heparinized blood to nonendothelial cell surfaces, followed by reinfusion and circulation within the body, greatly magnifies this response in cardiac surgery with CPB. Off-pump cardiac surgery does not solve postoperative inflammatory reactions and alterations of lung function.
Furthermore, many surgical procedures still need extracorporeal circulation (ECC). Thus, ECC technology has to improve and new research is needed to control the biologic reactions triggered by ECC and to develop improved biocompatibility. Evidence-based advances need experimental research and thus animal models. Of course, large animal models are closer to clinical practice, but because they are very expensive, most series involving large animals remain rather small.
Shao and colleagues [1] have used a clinically relevant in vivo model of rat CPB to study various aspects of CPB-mediated inflammation. They demonstrate that pretreatment with simvastatin may largely suppress the inflammatory lung response to ECC. The importance of their approach is somewhat mitigated because no sternotomy nor aortic cross-clamping was performed. Their experimental setup, however, does allow the specific influence of ECC without the influence of surgery to be investigated.
A reproducible model for CPB in rats may also facilitate studies on molecular mechanisms responsible for the inflammatory response to ECC and new pharmacologic approaches because larger numbers of subjects and disease models are possible. It is remarkable that an anticholesterol drug displays an unsuspected antiinflammatory role that is completely unrelated to cholesterol manipulation. Many studies have reported a prominent role of inflammation and immune responses in atherosclerosis, and therapeutic strategies, including statins to reduce inflammation, may exert beneficial effects in the prevention of atherosclerotic progression.
The work by Shao and colleagues adds new evidence regarding statins as antiinflammatory agents in the context of ECC. Therefore the inflammatory pathways and mediators affected by 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors during ECC deserve further investigation. Because leukocyte/endothelial interaction and activation of inflammatory cells occurs during ECC, statins may interfere with a proinflammatory pathway of adhesion and migration at levels of protein expression and function.
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