Remote ischemic preconditioning attenuates cardiopulmonary bypass-induced lung injury

Zhou, Xiaona; Jiang, Run-Zhu; Dong, Yucai; Wang, Lifeng

doi:10.1371/journal.pone.0189501

Cited by 33 publications

(22 citation statements)

References 21 publications

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“…During the experiment, the rectal temperature was monitored and maintained within 36-38°C by a heat blanket. The flow rate was gradually adjusted to 100 ml/kg body weight/min and maintained for 60 min [17]. During CPB, the mean arterial pressure was maintained within the range of 60 to 80 mmHg using the continuous injection of adrenaline.…”

Section: In Vivo Experiments Rat Cpb Modelmentioning

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: In Vivo Experiments Rat Cpb Modelmentioning

confidence: 99%

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

et al. 2020

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“…During the experiment, the rectal temperature was monitored and maintained within 36-38 ℃ by a heat blanket. The flow rate was gradually adjusted to 100 ml/kg body weight/min and maintained for 60 min [17]. During CPB, the mean arterial pressure was maintained within the range of 60 to 80 mmHg using the continuous injection of adrenaline.…”

Section: Rat Cpb Modelmentioning

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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“…RIC has proven effective at attenuating pro-inflammatory cytokine release in animal models of cerebral infarction, renal, pulmonary and hepatic reperfusion injury [ 31 , 70 , 83 , 145 , 156 ]. In a population of aged rats undergoing middle cerebral artery occlusion (mCAO), RIC significantly reduced levels of IL-1, IL-6 and IFN-γ in both plasma and the brain, whilst reducing the expression of hypoxia inducible factor (HIF-1α).…”

Section: Cytokines In Myocardial Infarction and Infectionmentioning

confidence: 99%

Does remote ischaemic conditioning reduce inflammation? A focus on innate immunity and cytokine response

Pearce¹,

Davidson²,

Yellon³

2021

Basic Res Cardiol

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The benefits of remote ischaemic conditioning (RIC) have been difficult to translate to humans, when considering traditional outcome measures, such as mortality and heart failure. This paper reviews the recent literature of the anti-inflammatory effects of RIC, with a particular focus on the innate immune response and cytokine inhibition. Given the current COVID-19 pandemic, the inflammatory hypothesis of cardiac protection is an attractive target on which to re-purpose such novel therapies. A PubMed/MEDLINE™ search was performed on July 13th 2020, for the key terms RIC, cytokines, the innate immune system and inflammation. Data suggest that RIC attenuates inflammation in animals by immune conditioning, cytokine inhibition, cell survival and the release of anti-inflammatory exosomes. It is proposed that RIC inhibits cytokine release via a reduction in nuclear factor kappa beta (NF-κB)-mediated NLRP3 inflammasome production. In vivo, RIC attenuates pro-inflammatory cytokine release in myocardial/cerebral infarction and LPS models of endotoxaemia. In the latter group, cytokine inhibition is associated with a profound survival benefit. Further clinical trials should establish whether the benefits of RIC in inflammation can be observed in humans. Moreover, we must consider whether uncomplicated MI and elective surgery are the most suitable clinical conditions in which to test this hypothesis.

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Remote ischemic preconditioning attenuates cardiopulmonary bypass-induced lung injury

Cited by 33 publications

References 21 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

Does remote ischaemic conditioning reduce inflammation? A focus on innate immunity and cytokine response

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