Inflammatory response and cardioprotection during open‐heart surgery: the importance of anaesthetics

Abstract

Open-heart surgery triggers an inflammatory response that is largely the result of surgical trauma, cardiopulmonary bypass, and organ reperfusion injury (e.g. heart). The heart sustains injury triggered by ischaemia and reperfusion and also as a result of the effects of systemic inflammatory mediators. In addition, the heart itself is a source of inflammatory mediators and reactive oxygen species that are likely to contribute to the impairment of cardiac pump function. Formulating strategies to protect the heart during open heart surgery by attenuating reperfusion injury and systemic inflammatory response is essential to reduce morbidity. Although many anaesthetic drugs have cardioprotective actions, the diversity of the proposed mechanisms for protection (e.g. attenuating Ca 2 þ overload, anti-inflammatory and antioxidant effects, pre-and post-conditioning-like protection) may have contributed to the slow adoption of anaesthetics as cardioprotective agents during open heart surgery. Clinical trials have suggested at least some cardioprotective effects of volatile anaesthetics. Whether these benefits are relevant in terms of morbidity and mortality is unclear and needs further investigation. This review describes the main mediators of myocardial injury during open heart surgery, explores available evidence of anaesthetics induced cardioprotection and addresses the efforts made to translate bench work into clinical practice.

Proinflammatory and Anti-Inflammatory Cytokine Balance in Patients With Cirrhotic Hepatitis During Live-Donor Liver Transplant

“…[8][9][10] This study demonstrated this condition; the secretion of IL-6 (a proinflammatory cytokine) increased markedly at the anhepatic stage, while the secretion of IL-10 (an antiinflammatory cytokine) was prominent at the neohepatic stage. Interleukin-6 is a cytokine actively secreted during major surgeries (eg, cardiopulmonary bypass), [11][12][13][14] and its concentration is closely related with postoperative prognosis. 15,16 Interleukin-10, which is secreted by activated helper T lymphocytes and induced by TNF-α secreted from monocytes, 17,18 suppresses the release of proinflammatory cytokines such as TNF-α, IL-1β, and IL-8.…”

Interleukin-6 in cardiac surgery

“…Glucagon-like peptide-1, an incretin hormone, was found to reduce circulating IL-6 levels in humans (48). Ischemic conditioning (pre and post) is a potential protective measure for prolonged ischemia and associated cytokine release (43). Plasma filtration was successful in cytokine removal but was associated with albumin loss.…”

“…The risk factors triggering IL-6 activities may include increasing age (in particular older age >70 years), obesity, atherosclerosis, diabetes (42), hepatic and renal dysfunction, high postoperative oxygen consumption and adrenaline infusions (43), etc.…”

Perioperative Organ Protection in Cardiac Surgery

“…Several membrane receptors seems to be involved in the phenomenon of ischemic preconditioning including -1, , opioid and adenosine receptors (19). In cardiac surgery, the observed systemic inflammatory response is the result of direct surgical trauma, ischemia-reperfusion injury and extracorporeal circulation (20) and cardiac injury can be triggered by ischemia, reperfusion, and also by local effects of mediators of the inflammatory response. Additionally, the heart itself may release locally inflammatory mediators and oxygen free radicals that can contribute to the worsening of the cardiac function.…”