Limb ischemic preconditioning attenuates acute lung injury in haemorrhagic shock/resuscitation rats

2011 ◽  
Vol 28 ◽  
pp. 170
Author(s):  
C. J. Huang ◽  
P. S. Tsai ◽  
W. C. Jan ◽  
C. H. Chen
Resuscitation ◽  
2013 ◽  
Vol 84 (3) ◽  
pp. 397-398
Author(s):  
Hsi-Ning Chu ◽  
Pei-Shan Tsai ◽  
Tao-Yeuan Wang ◽  
Chun-Jen Huang

Resuscitation ◽  
2009 ◽  
Vol 80 (10) ◽  
pp. 1204-1210 ◽  
Author(s):  
Chen-Hsien Yang ◽  
Pei-Shan Tsai ◽  
Tao-Yeuan Wang ◽  
Chun-Jen Huang

Resuscitation ◽  
2011 ◽  
Vol 82 (1) ◽  
pp. 97-104 ◽  
Author(s):  
Hsi-Ning Chu ◽  
Pei-Shan Tsai ◽  
Tao-Yeuan Wang ◽  
Chun-Jen Huang

2020 ◽  
Vol 5 (1) ◽  

We are describing a case of acute lung injury associated with uraemia and haemorrhagic shock. The treatment has consisted of the administration of repeated and equal doses of exogenous surfactant for 72 hours, starting within 48 hours from the beginning of the symptoms. A rapid improvement in the lung function has been detected, with consequent weaning from mechanical ventilation. The CT scan has confirmed the enhancement of atelectasis and hypoventilation. This case highlights the pivotal role of the administration of exogenous surfactant in selected cases of acute lung injury. If an anti-inflammatory effect is needed, we suppose that a repeated treatment with fractional dose is more effective.


Resuscitation ◽  
2011 ◽  
Vol 82 (6) ◽  
pp. 760-766 ◽  
Author(s):  
Woan-Ching Jan ◽  
Cay-Huyen Chen ◽  
Pei-Shan Tsai ◽  
Chun-Jen Huang

2019 ◽  
Vol 47 (2) ◽  
pp. 936-950 ◽  
Author(s):  
Yun-Hee Kim ◽  
Young-Sung Kim ◽  
Byung-Hwa Kim ◽  
Kuen-Su Lee ◽  
Hyung-Sun Park ◽  
...  

Objective Acute lung injury is responsible for mortality in seriously ill patients. Previous studies have shown that systemic inflammation is attenuated by remote ischemic preconditioning (RIPC) via reducing nuclear factor-kappa B (NF-κB). Therefore, we investigated whether lipopolysaccharide (LPS)-induced indirect acute lung injury (ALI) can be protected by RIPC. Methods RIPC was accomplished by 10 minutes of occlusion using a tourniquet on the right hind limb of mice, followed by 10 minutes of reperfusion. This process was repeated three times. Intraperitoneal LPS (20 mg/kg) was administered to induce indirect ALI. Inflammatory cytokines in bronchoalveolar lavage fluid were analyzed using an enzyme-linked immunosorbent assay. Pulmonary tissue was excised for histological examination, and for examining NF-κB activity and phosphorylation of inhibitor of κBα (IκBα). Results NF-κB activation and LPS-induced histopathological changes in the lungs were significantly alleviated in the RIPC group. RIPC reduced phosphorylation of IκBα in lung tissue of ALI mice. Conclusions RIPC attenuates endotoxin-induced indirect ALI. This attenuation might occur through modification of NF-κB mediation of cytokines by modulating phosphorylation of IκBα.


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