Controlled lung reperfusion to reduce pulmonary ischaemia/reperfusion injury after cardiopulmonary bypass in a porcine model

Slottosch, Ingo; Liakopoulos, Oliver J.; Kuhn, Elmar; Deppe, A.-C.; Lopez‐Pastorini, Alberto; Schwarz, David; Neef, Klaus; Choi, Yeong‐Hoon; Jung, Kristina; Mühlfeld, Christian; Wahlers, Thorsten

doi:10.1093/icvts/ivu270

Cited by 17 publications

(11 citation statements)

References 25 publications

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“…During CPB, lung ischaemia and the introduction of an artificial circuit into the blood resulted in severe local and systemic inflammation [20], which led to prolonged mechanical ventilation, a prolonged stay in the ICU and even respiratory failure and increased mortality. ECFCs can reduce the ventilator-induced lung injury in rats with ARDS and protect against renal reperfusion injury via anti-inflammatory effects [10,11].…”

Section: Discussionmentioning

confidence: 99%

Endothelial colony-forming cells reduced the lung injury induced by cardiopulmonary bypass in rats

et al. 2020

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Background: Cardiopulmonary bypass (CPB) results in severe lung injury via inflammation and endothelial injury. The aim of this study was to evaluate the effect of endothelial colony-forming cells (ECFCs) on lung injury in rats subjected to CPB. Methods: Thirty-two rats were randomized into the sham, CPB, CPB/ECFC and CPB/ECFC/L-NIO groups. The rats in the sham group received anaesthesia, and the rats in the other groups received CPB. The rats also received PBS, ECFCs and L-NIO-pre-treated ECFCs. After 24 h of CPB, pulmonary capillary permeability, including the PaO 2 /FiO 2 ratio, protein levels in bronchoalveolar lavage fluid (BALF) and lung tissue wet/dry weight were evaluated. The cell numbers and cytokines in BALF and peripheral blood were tested. Endothelial injury, lung histological injury and apoptosis were assessed. The oxidative stress response and apoptosis-related proteins were analysed. Results: After CPB, all the data deteriorated compared with those obtained in the S group (sham vs CPB vs CPB/ ECFC vs CPB/ECFC/L-NIO: histological score 1.62 ± 0.51 vs 5.37 ± 0.91 vs 3.37 ± 0.89 vs 4.37 ± 0.74; PaO 2 /FiO 2 389 ± 12 vs 233 ± 36 vs 338 ± 28 vs 287 ± 30; wet/dry weight 3.11 ± 0.32 vs 6.71 ± 0.73 vs 4.66 ± 0.55 vs 5.52 ± 0.57; protein levels in BALF: 134 ± 22 vs 442 ± 99 vs 225 ± 41 vs 337 ± 53, all P < 0.05). Compared to the CPB treatment, ECFCs significantly improved pulmonary capillary permeability and PaO 2 /FiO 2. Similarly, ECFCs also decreased the inflammatory cell number and pro-inflammatory factors in BALF and peripheral blood, as well as the oxidative stress response in the lung tissue. ECFCs reduced the lung histological injury score and apoptosis and regulated apoptosis-related proteins in the lung tissue. Compared with the CPB/ECFC group, all the indicators were partly reversed by the L-NIO. Conclusions: ECFCs significantly reduced lung injury induced by inflammation after CPB.

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Section: Discussionmentioning

confidence: 99%

Endothelial colony-forming cells reduced the lung injury induced by cardiopulmonary bypass in rats

et al. 2020

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“…During CPB, lung ischaemia and the introduction of an artificial circuit into the blood resulted in severe local and systemic inflammation [20], which led to prolonged mechanical ventilation, a prolonged stay in the ICU, and even respiratory failure and increased mortality. ECFCs can reduce the ventilator-induced lung injury in rats with ARDS and protect against renal reperfusion injury via antiinflammatory effects [10] [11].…”

Section: Discussionmentioning

confidence: 99%

Endothelial colony-forming cells reduced the lung injury induced by cardiopulmonary bypass in rats

Sun

Zhao

Tai

et al. 2020

Preprint

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Background: Cardiopulmonary bypass (CPB) results in severe lung injury via inflammation and endothelial injury. The aim of this study was to evaluate the effect of endothelial colony-forming cells (ECFCs) on lung injury in rats subjected to CPB. Methods: Thirty-two rats were randomized into the sham, CPB, CPB/ECFC and CPB/ECFC/L-NIO groups. The rats in the sham group received anaesthesia, and the rats in the other groups received CPB. The rats also received PBS, ECFCs and L-NIO-pretreated ECFCs. After 24 hours of CPB, pulmonary capillary permeability, including the PaO 2 /FiO 2 ratio, protein levels in bronchoalveolar lavage fluid (BALF) and lung tissue wet/dry weight, was evaluated. The cell numbers and cytokines in BALF and peripheral blood were tested. Endothelial injury, lung histological injury and apoptosis were assessed. The oxidative stress response and apoptosis-related proteins were analysed. Results: After CPB, all the data deteriorated compared with those obtained in the S group (sham vs CPB vs CPB/ECFC vs CPB/ECFC/L-NIO: histological score: 1.62±0.51 vs 5.37±0.91 vs 3.37±0.89 vs 4.37±0.74; PaO 2 /FiO 2 : 389±12 vs 233±36 vs 338±28 vs 287±30; wet/dry weight: 3.11±0.32 vs 6.71±0.73 vs 4.66±0.55 vs 5.52±0.57; protein levels: 134±22 vs 442±99 vs 225±41 vs 337±53, all P<0.05). Compared to the CPB treatment, ECFCs significantly improved pulmonary capillary permeability and PaO 2 /FiO 2 . Similarly, ECFCs also decreased the inflammatory cell number and pro-inflammatory factors in BALF and peripheral blood, as well as the oxidative stress response in the lung tissue. ECFCs reduced the lung histological injury score and apoptosis and regulated apoptosis-related proteins in the lung tissue. Compared with CPB/ECFC group, all the indicators were partly reversed by the L-NIO. Conclusions: ECFCs significantly reduced lung injury induced by inflammation after CPB.

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“…It seems to be remarkable that despite an appropriate “cardiac output” delivered by the heart-lung-machine and body cooling, organ injuries develop, which impair the post-operative result. Moreover, both bypassed organs -heart and lung- are burdened with ischemia and reperfusion injury, which also has a negative impact on the post-operative outcome (Royster, 1993 ; Slottosch et al, 2014 ).…”

Section: Introductionmentioning

confidence: 99%

Strategies for Pharmacological Organoprotection during Extracorporeal Circulation Targeting Ischemia-Reperfusion Injury

Salameh

Dhein

2015

Front. Pharmacol.

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Surgical correction of congenital cardiac malformations or aortocoronary bypass surgery in many cases implies the use of cardiopulmonary-bypass (CPB). However, a possible negative impact of CPB on internal organs such as brain, kidney, lung and liver cannot be neglected. In general, CPB initiates a systemic inflammatory response (SIRS) which is presumably caused by contact of blood components with the surface of CPB tubing. Moreover, during CPB the heart typically undergoes a period of cold ischemia, and the other peripheral organs a global low flow hypoperfusion. As a result, a plethora of pro-inflammatory mediators and cytokines is released activating different biochemical pathways, which finally may result in the occurrence of microthrombosis, microemboli, in depletion of coagulation factors and haemorrhagic diathesis besides typical ischemia-reperfusion injuries. In our review we will focus on possible pharmacological interventions in patients to decrease negative effects of CPB and to improve post-operative outcome with regard to heart and other organs like brain, kidney, or lung.

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Controlled lung reperfusion to reduce pulmonary ischaemia/reperfusion injury after cardiopulmonary bypass in a porcine model

Cited by 17 publications

References 25 publications

Endothelial colony-forming cells reduced the lung injury induced by cardiopulmonary bypass in rats

Endothelial colony-forming cells reduced the lung injury induced by cardiopulmonary bypass in rats

Endothelial colony-forming cells reduced the lung injury induced by cardiopulmonary bypass in rats

Strategies for Pharmacological Organoprotection during Extracorporeal Circulation Targeting Ischemia-Reperfusion Injury

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