scholarly journals Extracorporeal Circulation in Cardiac Surgery: Inflammatory response, controversies and Future Directions

2019 ◽  
Vol 13 (2) ◽  
pp. 158-173 ◽  
Author(s):  
Omar Giacinto ◽  
Umberto Satriano ◽  
Antonio Nenna ◽  
Cristiano Spadaccio ◽  
Mario Lusini ◽  
...  

Background: Endothelial injury occurring during cardiopulmonary bypass is a major contributing factor in the development of organ dysfunction, which leads to many of the postoperative complications occurring during cardiac surgery. Objective: This narrative review aims to summarize the main mechanisms of cardiopulmonary bypass - related disease, evaluating the unfavorable events leading to tissue injury, with a description of current pharmacologic and non-pharmacologic mechanisms to reduce CPB-related injury. Methods: A Medline/Pubmed/Scopus search was conducted using clinical queries with the key terms "cardiac surgery", “cardiopulmonary bypass”, "inflammation" and “endothelial injury”, and related MeSH terms, until July 2019. The search strategy included meta-analyses, randomized controlled trials, clinical trials, reviews and pertinent references. Patents were searched using the same key terms from https://patents.google.com/, www.uspto.gov, and www.freepatentsonline.com. Results: In this review, we discuss the current knowledge of the mechanisms of vascular endothelial cell injury, the acute inflammatory response, and the regulatory factors that control the extent of vascular injury during extracorporeal circulation, summarizing the main target of anti-inflammatory pharmacologic and non-pharmacologic strategies. Conclusion: Inflammatory response and endothelial dysfunction following cardiopulmonary bypass are the prices to pay for the benefits offered during cardiac surgery procedures. Counteracting the detrimental effect of extracorporeal circulation appears to be crucial to improve clinical outcomes in pediatric and adult cardiac surgery. The intrinsic complexity and the tight interplay of the factors involved might require a holistic approach against inflammation and endothelial response.


2008 ◽  
Vol 9 (6) ◽  
pp. 555-560 ◽  
Author(s):  
Salvatore Di Stefano ◽  
Elena Casquero ◽  
Rosa Bustamante ◽  
Juan Bustamante ◽  
Eduardo Tamayo ◽  
...  

2012 ◽  
Vol 60 (S 01) ◽  
Author(s):  
S Lehmann ◽  
J Garbade ◽  
J Seeburger ◽  
S Leontyev ◽  
S Dhein ◽  
...  

2012 ◽  
Vol 60 (S 01) ◽  
Author(s):  
R Kubicki ◽  
J Grohmann ◽  
J Kroll ◽  
M Siepe ◽  
F Humburger ◽  
...  

2013 ◽  
Vol 61 (S 01) ◽  
Author(s):  
TE Siegle ◽  
I Friedrich ◽  
A Paraforos ◽  
G Haimerl ◽  
W Olmscheid ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Qian Gong ◽  
Zhi-ming Shen ◽  
Zhe Sheng ◽  
Shi Jiang ◽  
Sheng-lin Ge

AbstractThe occurrence of cardiac surgery-associated acute kidney injury (CSA-AKI) increases hospital stay and mortality. MicroRNAs has a crucial role in AKI. This objective of the current study is to explore the function of hsa-miR-494-3p in inflammatory response in human kidney tubular epithelial (HK2) cells with hypoxia/reoxygenation. According to KDIGO standard, patients after cardiac surgery with cardiopulmonary bypass were divided into two groups: AKI (n = 10) and non-AKI patients (n = 8). HK2 were raised in the normal and hypoxia/reoxygenation circumstances and mainly treated by overexpression ofmiR-494-3p and HtrA3. The relationship between miR-494-3p and HtrA3 was determined by dual-luciferase reporter assay. Our result showed that Hsa-miR-494-3p was elevated in the serum of patients with CSA-AKI, and also induced in hypoxic reoxygenated HK2 cells. Hsa-miR-494-3p also increased a hypoxia-reoxygenation induced inflammatory response in HK2 cells. Moreover, as a target gene of miR-494-3p, overexpression of HtrA3 downregulated the hypoxia-reoxygenation induced inflammatory response in HK2 cells. Overexpression of hsa-miR-494-3p-induced inflammatory response was inhibited by overexpression of HtrA3. Collectively, we identified that hsa-miR-494-3p, a miRNA induced in both circulation of AKI patients and hypoxia-reoxygenation-treated HK2 cells, enhanced renal inflammation by targeting HtrA3, which may suggest a possible role as a new therapeutic target for CSA-AKI.


Trials ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Thiago Augusto Azevedo Maranhão Cardoso ◽  
Gudrun Kunst ◽  
Caetano Nigro Neto ◽  
José de Ribamar Costa Júnior ◽  
Carlos Gustavo Santos Silva ◽  
...  

Abstract Background Recent experimental evidence shows that sevoflurane can reduce the inflammatory response during cardiac surgery with cardiopulmonary bypass. However, this observation so far has not been assessed in an adequately powered randomized controlled trial. Methods We plan to include one hundred patients undergoing elective coronary artery bypass graft with cardiopulmonary bypass who will be randomized to receive either volatile anesthetics during cardiopulmonary bypass or total intravenous anesthesia. The primary endpoint of the study is to assess the inflammatory response during cardiopulmonary bypass by measuring PMN-elastase serum levels. Secondary endpoints include serum levels of other pro-inflammatory markers (IL-1β, IL-6, IL-8, TNFα), anti-inflammatory cytokines (TGFβ and IL-10), and microRNA expression in peripheral blood to achieve possible epigenetic mechanisms in this process. In addition clinical endpoints such as presence of major complications in the postoperative period and length of hospital and intensive care unit stay will be assessed. Discussion The trial may determine whether adding volatile anesthetic during cardiopulmonary bypass will attenuate the inflammatory response. Trial registration ClinicalTrials.gov NCT02672345. Registered on February 2016 and updated on June 2020.


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