Cardiopulmonary Bypass and Oxidative Stress

Abstract

The development of the cardiopulmonary bypass (CPB) revolutionized cardiac surgery and contributed immensely to improved patients outcomes. CPB is associated with the activation of different coagulation, proinflammatory, survival cascades and altered redox state. Haemolysis, ischaemia, and perfusion injury and neutrophils activation during CPB play a pivotal role in oxidative stress and the associated activation of proinflammatory and proapoptotic signalling pathways which can affect the function and recovery of multiple organs such as the myocardium, lungs, and kidneys and influence clinical outcomes. The administration of agents with antioxidant properties during surgery either intravenously or in the cardioplegia solution may reduce ROS burst and oxidative stress during CPB. Alternatively, the use of modified circuits such as minibypass can modify both proinflammatory responses and oxidative stress.

Change in Free Radical and Antioxidant Enzyme Levels in the Patients Undergoing Open Heart Surgery with Cardiopulmonary Bypass

“…It is considered that various factors such as surgical damage, CPB, and ischemia-reperfusion damage cause oxidative stress in ONCABG patients [20]. Haemolysis occurring in CPB, ischemia-reperfusion damage, and activation of neutrophils are important factors in the formation of oxidative stress [2]. Pumping period in heart surgery and aortic cross clamp period are important factors in ischemia-reperfusion damage [21].…”

“…Superoxide anion (O 2 −∙ ), hydrogen peroxide (H 2 O 2 ), hydroxyl radical ( ∙ OH), and peroxynitrite (ONOO − ) are the essential ROS types that cause oxidative damage in the heart [2]. Open heart surgeries performed with cardiopulmonary bypass induce oxidative stress.…”

“…Also, cardiac surgical intervention makes the patients more susceptible to diabetes, renal and lung diseases related to oxidative stress, and also excess formation of redox [2]. …”

Promotion of anoxia‑reoxygenation‑induced inflammation and permeability enhancement by nicotinamide phosphoribosyltransferase‑activated MAPK signaling in human umbilical vein endothelial cells

“…It has been demonstrated that MAPK signaling is activated during CPB-triggered acute lung injury, and mediates cellular inflammation and permeability (20). Thus, the present study tested the phosphorylation of p38 MAPK and ERK to investigate the regulation of MAPK signaling by NAMPT under A-R treatment.…”

Inflammation, oxidative stress and postoperative atrial fibrillation in cardiac surgery

“…It exposes RBCs to non-physiological stimuli modifying their integrity and role. CPB can damage RBC due to shear stress forces which make RBC less deformable and more fragile (J. F. Hoffman, 1962;Morariu, et al, 2004), thereby resulting in more free Hb in circulation (Baskurt & Meiselman, 2003;Morariu, et al, 2004;Saraf, Wellsted, Sharma, & Gorog, 2009;Zakkar, Guida, Suleiman, & Angelini, 2015). Furthermore; peri-operative blood transfusion can result in increased oxidative stress when stored blood is used due to diminish antioxidant properties or storage defect which is evident from ATP and 2,3-diphosphoglycerate depletion and increased lipid peroxidation (Karkouti, 2012;Relevy, Koshkaryev, Manny, Yedgar, & Barshtein, 2008;Zakkar, et al, 2015).…”