Role of Platelets in Acute Lung Injury after Extracorporeal Circulation in Cardiac Surgery Patients: A systemic review

2021 ◽  
pp. 101088
Author(s):  
Bhushan Sandeep ◽  
Zongwei Xiao ◽  
Fengying Zhao ◽  
Qianru Feng ◽  
Ke Gao
Keyword(s):  
Cardiac Surgery ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Extracorporeal Circulation ◽  
Systemic Review

scholarly journals The role of nitric oxide in treatment of acute lung injury after surgery with extracorporeal circulation

2003 ◽  
Vol 50 (2) ◽  
pp. 49-54 ◽  
Author(s):  
R. Sindjelic ◽  
G. Vlajkovic ◽  
Miljko Ristic ◽  
I. Divac ◽  
D. Markovic
Keyword(s):  
Nitric Oxide ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Extracorporeal Circulation ◽  
Demographic Data ◽  
Oxygenation Index ◽  
Mechanical Lung Ventilation ◽  
Group A ◽  
Group B

Postoperative acute lung injury (ALI) compromises oxygen transfer across alveolar-capillary membrane with consecutive hypoxia, one of its indicators being reduction of oxygenation index PaO2/FiO2 below 40 kPa (300 mm Hg). Management of ALI includes different procedures like mechanical lung ventilation (MLV), drugs and others. One of the new possibilities for treatment of ALI is nitric oxide (NO) inhalation. The aim of this prospective study was to examine the role of NO inhalation in treatment of ALI. 14 patients with ALI developed immediately after operation with extracorporeal circulation (ECC) were included in the study. Group A (n = 8) inhaled NO and group B (n = 6) did not inhale NO during treatment of ALI. All other therapeutic measures were the same in both groups. The groups were similar in relation to demographic data, type of surgery and duration of ECC. PaO2/FiO2 was calculated before operation (T1), immediately after surgery (T2) and after lung recovery, when the need for MLV stopped (T3). The duration of MLV was also registered. PaO2/FiO2 (kPa) in referent times was in group A 54,9 ? 1,6, 33,8 ? 1,2 and 46,2 ? 0,8 and in group B 52,2 ? 1,1, 33,5 ? 1,5 and 47,3 ? 0,9, respectively. There was a statistically significant decrease of PaO2/FiO2 in T2 and T3 vs T1 in both groups (p < 0,05), while the difference between the groups was not statistically significant. The duration of MLV (h) in group B (28,5 ? 1,6) was statistically significantly shorter than in group A (63,1 ? 8,7) (p < 0,01). According to the results of this study we conclude that NO inhalation during ALI after surgery with ECC significantly reduces the duration of MVL and improves pulmonary recovery .

scholarly journals Is there a role of TNFR1 in acute lung injury cases associated with extracorporeal circulation?

2014 ◽  
Vol 15 (3) ◽  
pp. 281-288
Author(s):  
Yu Zhao ◽  
Chong-wei Zhang ◽  
Wen-jing Zhou ◽  
Jiao Chen ◽  
Nan-fu Luo ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Extracorporeal Circulation

scholarly journals Leukocyte immunoglobulin-like receptor B4 deficiency exacerbates acute lung injury via NF-κB signaling in bone marrow-derived macrophages

2019 ◽  
Vol 39 (6) ◽  
Author(s):  
Tao Qiu ◽  
Jiangqiao Zhou ◽  
Tianyu Wang ◽  
Zhongbao Chen ◽  
Xiaoxiong Ma ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Stromal Cells ◽  
Marrow Cell ◽  
Marrow Transplant ◽  
Cell Source ◽  
Transplant Model ◽  
Acute Inflammatory Disease

AbstractAcute lung injury (ALI) is an acute inflammatory disease. Leukocyte immunoglobulin-like receptor B4 (LILRB4) is an immunoreceptor tyrosine-based inhibitory motif (ITIM)-bearing inhibitory receptor that is implicated in various pathological processes. However, the function of LILRB4 in ALI remains largely unknown. The aim of the present study was to explore the role of LILRB4 in ALI. LILRB4 knockout mice (LILRB4 KO) were used to construct a model of ALI. Bone marrow cell transplantation was used to identify the cell source of the LILRB4 deficiency-aggravated inflammatory response in ALI. The effect on ALI was analyzed by pathological and molecular analyses. Our results indicated that LILRB4 KO exacerbated ALI triggered by LPS. Additionally, LILRB4 deficiency can enhance lung inflammation. According to the results of our bone marrow transplant model, LILRB4 regulates the occurrence and development of ALI by bone marrow-derived macrophages (BMDMs) rather than by stromal cells in the lung. The observed inflammation was mainly due to BMDM-induced NF-κB signaling. In conclusion, our study demonstrates that LILRB4 deficiency plays a detrimental role in ALI-associated BMDM activation by prompting the NF-κB signal pathway.

H2O2 inhibits alveolar epithelial wound repair in vitro by induction of apoptosis

2004 ◽  
Vol 287 (2) ◽  
pp. L448-L453 ◽  
Author(s):  
Thomas Geiser ◽  
Masanobu Ishigaki ◽  
Coretta van Leer ◽  
Michael A. Matthay ◽  
V. Courtney Broaddus
Keyword(s):  
Acute Lung Injury ◽  
Epithelial Cells ◽  
Lung Injury ◽  
Cell Viability ◽  
Wound Repair ◽  
Wound Edge ◽  
Alveolar Epithelial ◽  
Induction Of Apoptosis

Reactive oxygen species (ROS) are released into the alveolar space and contribute to alveolar epithelial damage in patients with acute lung injury. However, the role of ROS in alveolar repair is not known. We studied the effect of ROS in our in vitro wound healing model using either human A549 alveolar epithelial cells or primary distal lung epithelial cells. We found that H2O2 inhibited alveolar epithelial repair in a concentration-dependent manner. At similar concentrations, H2O2 also induced apoptosis, an effect seen particularly at the edge of the wound, leading us to hypothesize that apoptosis contributes to H2O2-induced inhibition of wound repair. To learn the role of apoptosis, we blocked caspases with the pan-caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp (zVAD). In the presence of H2O2, zVAD inhibited apoptosis, particularly at the wound edge and, most importantly, maintained alveolar epithelial wound repair. In H2O2-exposed cells, zVAD also maintained cell viability as judged by improved cell spreading and/or migration at the wound edge and by a more normal mitochondrial potential difference compared with cells not treated with zVAD. In conclusion, H2O2 inhibits alveolar epithelial wound repair in large part by induction of apoptosis. Inhibition of apoptosis can maintain wound repair and cell viability in the face of ROS. Inhibiting apoptosis may be a promising new approach to improve repair of the alveolar epithelium in patients with acute lung injury.

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