Regulation of cytokine synthesis in cardiac surgery: Role of extracorporeal circuit and humoral mediators in vivo and in vitro

Abstract

(1) In patients, CPB induces early transient LPS hyporesponsiveness; (2) blood contact with foreign surfaces induces LPS hyporesponsiveness; (3) serum cytokine-inhibitory activities are released after CPB, but not in mock ECC. Impaired leukocyte function may explain increased susceptibility to infections after CPB.

Hsp70 and cardiac surgery: molecular chaperone and inflammatory regulator with compartmentalized effects

“…This reduces the risk of deteriorating effects of systemic inflammation to take place (e.g., circulatory failure, organ dysfunction). This model could also explain the more pronounced effects of on-pump cardiac surgery on postoperative downregulation of immune reactivity, compared to off-pump surgery (Borgermann et al 2007 Fig. 4 Model of the compartmentalized immunomodulatory effects of Hsp70 during localized versus systemic inflammatory stress.…”

Low‐frequency ventilation during cardiopulmonary bypass for lung protection: A randomized controlled trial

“…Severity ranges from mild atelectasis to life‐threatening acute lung injury (ALI) or respiratory failure requiring prolonged postoperative ventilation or adult respiratory distress syndrome (ARDS) . Harmful effects of CPB on pulmonary function persist despite advances in anesthetic techniques . Pulmonary dysfunction after cardiac surgery also affects clinical outcomes with increased morbidity, mortality and delayed discharge from hospital, leading to increasing in the health care resources used and their associated cost…”

Monocyte hyporesponsiveness and Toll-like receptor expression profiles in coronary artery bypass grafting and its clinical implications for postoperative inflammatory response and pneumonia

“…2,3 The early postoperative course of SIRS after CABG is characterised by hyperproduction of proinflammatory cytokines. 6 Several factors are considered responsible for perioperative inflammation, such as surgical trauma, 7-9 myocardial ischaemia-reperfusion damage after CPB, 10,11 blood contact with surfaces of the CPB, [12][13][14] or blood contact with the pericardial cavity. 6 Several factors are considered responsible for perioperative inflammation, such as surgical trauma, 7-9 myocardial ischaemia-reperfusion damage after CPB, 10,11 blood contact with surfaces of the CPB, [12][13][14] or blood contact with the pericardial cavity.…”

“…24 Chemokine IL-8 is representative for the link to the acquired immune system by its key function in chemotaxis. In patients undergoing cardiac surgery with CPB, monocyte hyporesponsiveness has been described, 12,[27][28][29] as well as a reduced surface expression of TLR-2 and TLR-4. 26 Circulating anti-inflammatory mediators can induce monocyte hyporesponsiveness, a decreased level of extracellular cytokine release in response to ex-vivo stimulation with pathogenic factors, in order to protect the body against an excessive immune response.…”