Pulmonary Perfusion With L-Arginine Ameliorates Post-Cardiopulmonary Bypass Lung Injury in a Rabbit Model

Chao, Yin‐Kai; Wu, Yu‐Chung; Yang, Kun Ju; Chiang, Ling Ling; Liu, Hui Ping; Lin, Pyng Jing; Chu, Yen

doi:10.1016/j.jss.2009.10.041

Cited by 11 publications

(10 citation statements)

References 23 publications

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“…Furthermore, it provides the possibility to establish organ protection strategies after circulatory arrest. A number of studies have been published on minimizing the damage of CPB and cardiac arrest on internal organs [ 45 – 57 ]. Cytokine measurements in prolonged CPB and moderate circulatory arrest allows the evaluation of immunological involvement and its effect on CPB-induced organ damage.…”

Section: Discussionmentioning

confidence: 99%

Blood cytokine expression correlates with early multi-organ damage in a mouse model of moderate hypothermia with circulatory arrest using cardiopulmonary bypass

et al. 2018

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Cardiopulmonary bypass (CPB) with moderate hypothermic cardiac arrest (MHCA) is essential for prolonged complex procedures in cardiac surgery and is associated with postoperative complications. Although cytokine release provoked through MHCA under CPB plays a pivotal role in postoperative organ damage, the pathomechanisms are unclear. Here, we investigated the cytokine release pattern and histological organ damage after MHCA using a recently described mouse CPB model. Eight BALB/c mice underwent 60 minutes of circulatory arrest under CPB, were successively rewarmed and reperfused. Blood cytokine concentrations and liver and kidney function parameters were measured and histological changes to these organs were compared to control animals. Our results showed a marked increase in proinflammatory cytokines and histological changes in the kidney, lung, and liver after CPB. Furthermore, clinical chemistry showed signs of hemolysis and acute kidney injury. These results suggest early onset of solid organ injury which correlates with increased leukocyte infiltration. A better understanding of the interplay between pro-inflammatory cytokine activation and solid organ injury in this model of CBP with MHCA will inform strategies to reduce organ damage during cardiac surgeries in the clinic.

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Section: Discussionmentioning

confidence: 99%

Blood cytokine expression correlates with early multi-organ damage in a mouse model of moderate hypothermia with circulatory arrest using cardiopulmonary bypass

et al. 2018

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“… 15 Currently, it was considered that systemic inflammatory response caused by the extracorporeal circulation and lung ischemia-reperfusion injury can lead to lung injury after extracorporeal circulation cardiac surgery. 16 - 18 Currently, the recognized possible mechanisms are: 1) ischemia-reperfusion injury results in reactive oxygen species and inflammatory molecules (especially cytokines) releasing into the circulation, 19 2) activation of white blood cells, platelets, complements and the blood coagulation system, and the releases of other inflammatory cytokines, which may be secondary to the contact of blood with extracorporeal circulation pipe, 20 and 3) relative insufficient visceral blood perfusion in intraoperative and postoperative can cause intestinal ischemia and increased capillary permeability, and this may lead to intestinal flora ectopicly entering into circulation. The pathophysiological process of DHCA is similar to the lung transplantation after cryopreserved process or the ischemia and reperfusion process of the lung.…”

Section: Discussionmentioning

confidence: 99%

Independent risk factors for hypoxemia after surgery for acute aortic dissection

Wei

Yang²,

Chi

et al. 2015

SMJ

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Objectives:To determine risk factors associated with postoperative hypoxemia after surgery for acute type A aortic dissection.Methods:We retrospectively analyzed the clinical data of 192 patients with acute type A aortic dissection who underwent surgery in Qingdao Municipal Hospital, Medical College of Qingdao University, Qingdao, China between January 2007 and December 2013. Patients were divided into hypoxemia group (n=55) [arterial partial pressure of oxygen (PaO2)/fraction of inspired oxygen (FiO2) ≤200 mm Hg] and non-hypoxemia group (n=137) [PaO2/FiO2 >200 mm Hg]. Perioperative clinical data were analyzed and compared between the 2 groups.Results:The incidence of postoperative hypoxemia after surgery for acute aortic dissection was 28.6% (55/192). Perioperative death occurred in 13 patients (6.8%). Multivariate regression identified body mass index (BMI) >25 kg/m2 (OR=21.929, p=0.000), deep hypothermic circulatory arrest (DHCA) (OR=11.551, p=0.000), preoperative PaO2/FiO2 ≤300 mm Hg (OR=7.830, p=0.000) and blood transfusion >6U in 24 hours postoperatively (OR=12.037, p=0.000) as independent predictors of postoperative hypoxemia for patients undergoing Stanford A aortic dissection surgery.Conclusion:Our study demonstrated that BMI >25 kg/m2, DHCA, preoperative PaO2/FiO2 ≤300 mm Hg, and blood transfusion in 24 hours postoperatively >6U were independent risk factors of the hypoxemia after acute type A aortic dissection aneurysm surgery.

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“…A-R has been reported to induce inflammation and enhance the cellular permeability of pulmonary vascular endothelial cells, which then led to pneumonedema, inducing hyoxemia, acute respiratory distress syndrome and even mortality (4). Thus, inhibiting inflammation and cellular permeability may improve the prognosis following CPB (5).…”

Section: Introductionmentioning

confidence: 99%

Promotion of anoxia‑reoxygenation‑induced inflammation and permeability enhancement by nicotinamide phosphoribosyltransferase‑activated MAPK signaling in human umbilical vein endothelial cells

et al. 2017

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Abstract. Previous studies have demonstrated that nicotinamide phosphoribosyltransferase (NAMPT) promoted inflammation and permeability of vascular endothelial cells following cardiopulmonary bypass (CPB). In addition, mitogen-activated protein kinase (MAPK) signaling was activated and contributed to these cell responses. However, the mechanism by which NAMPT regulates cellular inflammation and permeability remains unknown, and whether NAMPT regulates MAPK signaling during this process is also not clear. The present study established an anoxia-reoxygenation (A-R) model using human umbilical vein endothelial cells (HUVECs) and investigated the regulation of MAPK signaling by NAMPT by using small RNA transfection, ELISA and western blot analysis. The results demonstrated that A-R significantly induced the expression levels of NAMPT and cellular permeability-associated proteins, and the release of several inflammatory factors. Furthermore, calcium and MAPK signaling were evidently increased. When the A-R cells were transfected with NAMPT small interfering RNA, the expression of cellular permeability-associated proteins was downregulated, the release of inflammatory factors was decreased, and calcium and MAPK signaling was blocked. These data suggest that NAMPT may activate MAPK signaling to promote A-R-induced inflammation and permeability enhancement of HUVECs. Therefore, the current study indicates that NAMPT may be a potential drug target for A-R-induced endothelial cell injury subsequent to CPB.

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Pulmonary Perfusion With L-Arginine Ameliorates Post-Cardiopulmonary Bypass Lung Injury in a Rabbit Model

Cited by 11 publications

References 23 publications

Blood cytokine expression correlates with early multi-organ damage in a mouse model of moderate hypothermia with circulatory arrest using cardiopulmonary bypass

Blood cytokine expression correlates with early multi-organ damage in a mouse model of moderate hypothermia with circulatory arrest using cardiopulmonary bypass

Independent risk factors for hypoxemia after surgery for acute aortic dissection

Promotion of anoxia‑reoxygenation‑induced inflammation and permeability enhancement by nicotinamide phosphoribosyltransferase‑activated MAPK signaling in human umbilical vein endothelial cells

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