Hypothermia During Cardiopulmonary Bypass Increases Need for Inotropic Support but Does Not Impact Inflammation in Children Undergoing Surgical Ventricular Septal Defect Closure
Abstract:Minimizing the systemic inflammatory response caused by cardiopulmonary bypass is a major concern. It has been suggested that the perfusion temperature affects the inflammatory response. The aim of this prospective study was to compare the effects of moderate hypothermia (32°C) and normothermia (36°C) during cardiopulmonary bypass on markers of the inflammatory response and clinical outcomes (time on ventilator) after surgical closure of ventricular septal defects. During surgical closure of ventricular septal… Show more
“…Despite major improvements in circuit design, oxygenators and the advent of heparin-bonded surfaces, the inflammatory response to CPB remains a clinical concern. There have been several attempts to attenuate postoperative cytokine release including anti-inflammatory therapy 24 , modifications in the bypass circuit 25 or changing temperature management in CPB 26 .…”
The 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 represent a promising therapeutic strategy for clinical practice.
“…Despite major improvements in circuit design, oxygenators and the advent of heparin-bonded surfaces, the inflammatory response to CPB remains a clinical concern. There have been several attempts to attenuate postoperative cytokine release including anti-inflammatory therapy 24 , modifications in the bypass circuit 25 or changing temperature management in CPB 26 .…”
The 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 represent a promising therapeutic strategy for clinical practice.
“…18,20 Furthermore, after enhancing the perfusion temperature, the effect of the hypothermic sympathetic response and increased blood viscosity on the hemodynamic effects weakens, resulting in the requirement of a higher dose of vasoconstrictors to maintain satisfactory perfusion pressure. 18,21 In contrast to hypothermic CPB, the increase in perfusion temperature may increase the effective dose of the anesthetic drug. 22 In 2011, a Canadian survey showed that more than 90% of institutions involved maintained a core temperature of 32-34℃ during CPB.…”
This survey accurately reflects the current situation of temperature management during CPB in institutions with an annual surgical volume of >500 cases, but has, hereby, failed to properly represent the institutions with a lower annual surgical volume.
“…In the conditions of modern anesthetic technology and perfusion, a considerable amount of information has accumulated on various methods of preventing SIR, which are effective to a greater or lesser extent. We offer an overview of the most commonly used methods for the prevention of SIR (see Table 2) [43,[78][79][80][81][82][83][84][85][86][87][88][89].…”
Section: You Need To Know the Enemy By Sight Or How Not To Pass By De...mentioning
This chapter presents the current data on delirium in children in the postoperative period with the correction of congenital heart defects. The analysis of the causes of delirium, according to the literature data, pathophysiology, clinical signs, and methods of diagnosis of postoperative delirium, is shown. In addition, methods for the prevention of delirium in children during cardiac surgery are presented.
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