O-62 Methylprednisolone promotes endothelial dysfunction in patients operated under cardiopulmonary bypass

2011 ◽  
Vol 25 (3) ◽  
pp. S27
Author(s):  
Vladimir Lomivorotov ◽  
Andrey Kalinichenko ◽  
Igor Kornilov ◽  
Sergey Efremov ◽  
Vladimir Shmirev ◽  
...  
Keyword(s):  
Cardiopulmonary Bypass ◽  
Endothelial Dysfunction

scholarly journals Anti-C5a monoclonal antibody reduces cardiopulmonary bypass and cardioplegia-induced coronary endothelial dysfunction

1998 ◽  
Vol 116 (6) ◽  
pp. 1060-1068 ◽  
Author(s):  
Motohisa Tofukuji ◽  
Gregory L. Stahl ◽  
Azin Agah ◽  
Caroline Metais ◽  
Michael Simons ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Cardiopulmonary Bypass ◽  
Endothelial Dysfunction ◽  
Coronary Endothelial Dysfunction

scholarly journals Targeting of cell-free DNA by DNase I diminishes endothelial dysfunction and inflammation in a rat model of cardiopulmonary bypass

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Carolyn Weber ◽  
Alexander Jenke ◽  
Vasilena Chobanova ◽  
Mariam Yazdanyar ◽  
Agunda Chekhoeva ◽  
...  
Keyword(s):  
Cardiopulmonary Bypass ◽  
Endothelial Dysfunction ◽  
Adhesion Molecules ◽  
Therapeutic Strategy ◽  
Dnase I ◽  
Intercellular Adhesion Molecule ◽  
Control Group ◽  
Cell Free Dna ◽  
Free Dna ◽  
Group 3

AbstractThe use of cardiopulmonary bypass (CPB) results in the activation of leukocytes, release of neutrophil extracellular traps (NETs) and severe inflammation. We hypothesize that targeting of circulating cell-free DNA (cfDNA) by DNases might represent a feasible therapeutic strategy to limit CPB-associated side effects. Male Wistar rats (n = 24) underwent CPB with deep hypothermic circulatory arrest (DHCA) and were divided into 3 groups: control (group 1), one i.v. bolus DNase I before CPB start (group 2) and a second DNase I dose before reperfusion (group 3). We found a positive correlation between plasma cfDNA/NETs levels and compromised endothelial vasorelaxation after CPB. DNase I administration significantly diminished plasma cfDNA/NETs levels. Further, a dose-dependent improvement in endothelial function accompanied by significant reduction of circulating intercellular adhesion molecule (ICAM)-1 was observed. Rats of group 3 had significantly reduced plasma IL-6 levels and downregulated expression of adhesion molecules resulting in impaired leukocyte extravasation and reduced MPO activity in lungs. Mechanistically, digestion of NETs by DNase I significantly diminished NETs-dependent upregulation of adhesion molecules in human endothelial cells. Altogether, systemic DNase I administration during CPB efficiently reduced cfDNA/NETs-mediated endothelial dysfunction and inflammation and might represents a promising therapeutic strategy for clinical practice.

Differential Effects of Inhaled and Intravenous Sildenafil in the Prevention of the Pulmonary Endothelial Dysfunction Due to Cardiopulmonary Bypass

2008 ◽  
Vol 51 (1) ◽  
pp. 11-17 ◽  
Author(s):  
Marie-Claude Aubin ◽  
Steve Laurendeau ◽  
Arnaud Mommerot ◽  
Yoan Lamarche ◽  
André Denault ◽  
...  
Keyword(s):  
Cardiopulmonary Bypass ◽  
Endothelial Dysfunction ◽  
Differential Effects

Inflammatory Response and Endothelial Dysfunction Following Cardiopulmonary Bypass: Pathophysiology and Pharmacological Targets

2019 ◽  
Vol 13 (2) ◽  
pp. 158-173 ◽  
Author(s):  
Omar Giacinto ◽  
Umberto Satriano ◽  
Antonio Nenna ◽  
Cristiano Spadaccio ◽  
Mario Lusini ◽  
...  
Keyword(s):  
Cardiac Surgery ◽  
Cardiopulmonary Bypass ◽  
Endothelial Dysfunction ◽  
Inflammatory Response ◽  
Extracorporeal Circulation ◽  
Tissue Injury ◽  
Vascular Endothelial Cell ◽  
Endothelial Injury ◽  
Mesh Terms ◽  
Key Terms

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.

Cyclic GMP infusion prevents endothelial dysfunction and acute lung injury induced by cardiopulmonary bypass

2004 ◽  
Vol 21 (Supplement 32) ◽  
pp. 3
Author(s):  
A. Ruiz ◽  
I. Rovira ◽  
J. Martinez ◽  
A. Puente ◽  
C. Ayats ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Cardiopulmonary Bypass ◽  
Endothelial Dysfunction ◽  
Lung Injury ◽  
Cyclic Gmp

Cardiopulmonary bypass increases endothelial dysfunction after pulmonary ischaemia-reperfusion in an animal model

2020 ◽  
Author(s):  
Jean Selim ◽  
Mouad Hamzaoui ◽  
Inès Boukhalfa ◽  
Zoubir Djerada ◽  
Laurence Chevalier ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cardiopulmonary Bypass ◽  
Endothelial Dysfunction ◽  
Lung Transplantation ◽  
Immunosorbent Assay ◽  
Plasma Levels ◽  
Vascular Reactivity ◽  
Enzyme Linked Immunosorbent Assay ◽  
Ischaemia Reperfusion ◽  
The Impact

Abstract OBJECTIVES Endothelial dysfunction during ischaemia-reperfusion (IR) is a major cause of primary graft dysfunction during lung transplantation. The routine use of cardiopulmonary bypass (CPB) during lung transplantation remains controversial. However, the contribution of CPB to pulmonary endothelial dysfunction remains unclear. The objective was to investigate the impact of CPB on endothelial dysfunction in a lung IR rat model. METHODS Rats were allocated to 4 groups: (i) Sham, (ii) IR, (iii) CPB and (iv) IR-CPB. The primary outcome was the study of pulmonary vascular reactivity by wire myograph. We also assessed glycocalyx degradation by enzyme-linked immunosorbent assay and electron microscopy and both systemic and pulmonary inflammation by enzyme-linked immunosorbent assay and immunohistochemistry. Rats were exposed to 45 min of CPB and IR. We used a CPB model allowing femoro-femoral support with left pulmonary hilum ischaemia for IR. RESULTS Pulmonary endothelium-dependent relaxation to acetylcholine was markedly reduced in the IR-CPB group (10.7 ± 9.1%) compared to the IR group (50.5 ± 5.2%, P < 0.001), the CPB group (54.1 ± 4.7%, P < 0.001) and the sham group (80.8 ± 6.7%, P < 0.001), suggesting that the association of pulmonary IR and CPB increases endothelial dysfunction. In IR-CPB, IR and CPB groups, vasorelaxation was completely abolished when inhibiting nitric oxide synthase, suggesting that this relaxation process was mainly mediated by nitric oxide. We observed higher syndecan-1 plasma levels in the IR-CPB group in comparison with the other groups, reflecting an increased degradation of glycocalyx. We also observed higher systemic inflammation in the IR-CPB group as shown by the increased plasma levels of IL-1β, IL-10. CONCLUSIONS CPB significantly increased the IR-mediated effects on pulmonary endothelial dysfunction. Therefore, the use of CPB during lung transplantation could be deleterious, by increasing endothelial dysfunction.

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