• Takaaki Suzuki.
• Department of Pediatric Cardiac Surgery, Saitama International Medical Center, and Saitama Medical University, Hidaka-shi, Saitama, Japan.
• Ann Thorac Cardiovasc Surg. 2010 Jun 1;16(3):150-5.

AbstractPostoperative cardiopulmonary bypass (CPB)-induced lung dysfunction still remains as a serious complication that could lead to life-threatening problems. CPB is associated with a whole-body inflammatory response. The contact of blood components with the artificial surface of the bypass circuit causes activation of complements, upregulation of cytokines and adhesion molecules, and induction of oxygen-free radicals. The pathogenic consequences are adhesions of complement-activated neutrophils to endothelial cells, neutrophil migration into the extravascular spaces, and free-radical mediated pulmonary damage. Injured endothelial cells are vulnerable to the cytokine-mediated inflammatory cascade. Moreover, CPB renders the lung being at risk for ischemic insults because lung perfusion is maintained solely by the bronchial arterial system. Postischemic reperfusion of the lung upregulates adhesion molecules and enhances neutrophil-endothelial cell adhesion and extravascular neutrophil sequestration, thereby aggravating further structural and functional abnormalities of pulmonary endothelial cells. Thus the systemic inflammatory response and ischemia-reperfusion during CPB constitute a vicious network in the pathogenesis of CPB-derived lung injury. Accordingly, it is postulated that additional pulmonary perfusion could alleviate CPB-induced lung damage. This review article summarizes recent literature on the mechanisms involved in lung dysfunction after CPB, and it also summarizes current reports on lung-protective perfusion techniques.

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