Limb Remote Ischemic Preconditioning Attenuates Lung Injury after Pulmonary Resection under Propofol–Remifentanil Anesthesia

Cai, Li; Xu, Ming; Wu, Yan; Li, Yunsheng; Huang, Wenqi; Liu, Ke-Xuan

doi:10.1097/aln.0000000000000266

Cited by 83 publications

(79 citation statements)

References 48 publications

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“…Also, they proposed the changes of TNF-a expression as a result of RPEC in the liver. 10 The protective effect of limb remote conditioning in lung injury after pulmonary resection was associated by decreased serum level of TNF-a and IL-6 in a randomized control trial study by Li et al 22 Taken together, these studies support a possible role for TNF-a in short-time ischemic conditioning treatment. IL-6 which is released by macrophages in the site of ischemia increases renal inflammation by recruiting more neutrophils into the injured kidney, stimulation of neutrophil release from the bone marrow, 23 prevention of neutrophil apoptosis and activation of neutrophils to produce toxic enzymes.…”

Section: 10supporting

confidence: 57%

Hind limb perconditioning renoprotection by modulation of inflammatory cytokines after renal ischemia/reperfusion

et al. 2016

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Purpose Renal ischemia/reperfusion (I/R) injury is a common clinical problem associated with significant mortality and morbidity. One newly described strategy to reduce this damage is remote perconditioning (RPEC), in which short-time ischemia of a limb during renal ischemia reduces the I/ R-induced kidney injury. This study aimed to assess whether RPEC confer protection through changes in pro-inflammatory mediators. Methods Rats were subjected to right nephrectomy and randomized into: sham (no intervention), I/R (subjected to 45-min left renal ischemia) and RPEC group (subjected to four cycles of 5-min I/R of the femoral artery administered during renal ischemia). After 24-h, blood, urine, and kidney samples were collected. Biochemical indicators of renal dysfunction were measured in the cases of Neutrophil gelatinase-associated lipocalin (NGAL), and N-acetyl-B-diglucosaminidase (NAG) activity. Inflammatory cytokines [interleukin (IL)-6 and tumor necrosis factor-alpha, TNF-a] expression in the renal tissues as well as Periodic acid-Schiff stained histological sections were evaluated. Results I/R resulted in renal dysfunction, as evidenced by higher renal NGAL expression and urinary NAG activities. This was accompanied by increased TNF-a and IL-6 expressions as well as histological changes in this group. However, RPEC improved renal histology and function compared with the I/R group. Furthermore, the RPEC group showed decreases in TNF-a and IL-6 expression. Conclusions These results suggest that RPEC reduces the dysfunction and injury associated with I/R of the kidney. This technique reduced the proinflammatory cytokine in the kidney. RPEC could be a promising strategy against I/R-induced acute kidney injury partly by down-regulation of inflammatory mediators. ARTICLE HISTORY

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Section: 10supporting

confidence: 57%

Hind limb perconditioning renoprotection by modulation of inflammatory cytokines after renal ischemia/reperfusion

et al. 2016

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“…Although restoration of blood flow to intestinal ischemic tissue is critical for tissue salvage, reperfusion also introduces inflammatory changes that exacerbate injury [12] . IP is a simple procedure conferring cytoprotection in critical organs that has clinical applications [13,14] . Although intestinal IP triggers powerful protective effects mechanisms by which it alleviates intestinal injury remain to be elucidated.…”

Section: Discussionmentioning

confidence: 99%

Ischemic preconditioning ameliorates intestinal injury induced by ischemia-reperfusion in rats

Wang

et al. 2015

WJG

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“…This technique has been applied successfully in patients undergoing a lobectomy and reduced oxidative stress levels in the peripheral circulation, decreased ALI incidence and resulted in earlier patient discharge (97).…”

Section: Ischemic Preconditioningmentioning

confidence: 99%

Oxidative and nitrosative stress during pulmonary ischemia-reperfusion injury: from the lab to the OR

Gielis¹,

Beckers²,

Briedé³

et al. 2017

Ann. Transl. Med.

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Oxidative and nitrosative stress are an umbrella term for pathophysiological processes that involve free radical generation during inflammation. In this review, the involvement of reactive oxygen and nitrogen species is evaluated during lung ischemia-reperfusion injury (LIRI) from a surgical point of view. The main biochemical and cellular mechanisms behind free radical generation are discussed, together with surgical procedures that may cause reperfusion injury. Finally, different therapeutic strategies are further explored. A literature search was performed, searching for "lung ischemia reperfusion injury", "reperfusion injury", "large animal model" and different search terms for each section: "surgery", "treatment", "cellular mechanism", or "enzyme". Although reperfusion injury is not an uncommon entity and there is a lot of evidence concerning myocardial ischemia-reperfusion injury, in the lung this phenomenon is less extensively described and studies in large animals are not easy to come by. With increasing number of patients on waiting lists for lung transplant, awareness for this entity should all but rise.

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Limb Remote Ischemic Preconditioning Attenuates Lung Injury after Pulmonary Resection under Propofol–Remifentanil Anesthesia

Abstract: Limb RIPC attenuates acute lung injury via improving intraoperative pulmonary oxygenation in patients without severe pulmonary disease after lung resection under propofol-remifentanil anesthesia.

Cited by 83 publications

References 48 publications

Hind limb perconditioning renoprotection by modulation of inflammatory cytokines after renal ischemia/reperfusion

Hind limb perconditioning renoprotection by modulation of inflammatory cytokines after renal ischemia/reperfusion

Ischemic preconditioning ameliorates intestinal injury induced by ischemia-reperfusion in rats

Oxidative and nitrosative stress during pulmonary ischemia-reperfusion injury: from the lab to the OR

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