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Anat Cell Biol. 2018 Jun;51(2):128-135. doi: 10.5115/acb.2018.51.2.128. Epub 2018 Jun 27.

The relationship between low survival and acute increase of tumor necrosis factor α expression in the lung in a rat model of asphyxial cardiac arrest.

Author information

1
Department of Emergency Medicine and Institute of Medical Sciences, Kangwon National University Hospital, Kangwon National University School of Medicine, Chuncheon, Korea.
2
Bio Safety Research Institute, College of Veterinary Medicine, Chonbuk National University, Iksan, Korea.
3
Department of Neurobiology, Kangwon National University School of Medicine, Chuncheon, Korea.
4
Department of Biomedical Science and Research Institute for Bioscience and Biotechnology, Hallym University, Chuncheon, Korea.
5
Department of Medical Education, Kangwon National University School of Medicine, Chuncheon, Korea.

Abstract

Cardiac arrest (CA) is sudden loss of heart function and abrupt stop in effective blood flow to the body. The patients who initially achieve return of spontaneous circulation (RoSC) after CA have low survival rate. It has been known that multiorgan dysfunctions after RoSC are associated with high morbidity and mortality. Most previous studies have focused on the heart and brain in RoSC after CA. Therefore, the aim of this research was to perform serological, physiological, and histopathology study in the lung and to determine whether or how pulmonary dysfunction is associated with low survival rate after CA. Experimental animals were divided into sham-operated group (n=14 at each point in time), which was not subjected to CA operation, and CA-operated group (n=14 at each point in time), which was subjected to CA. The rats in each group were sacrificed at 6 hours, 12 hours, 24 hours, and 2 days, respectively, after RoSC. Then, pathological changes of the lungs were analyzed by hematoxylin and eosin staining, Western blot and immunohistochemistry for tumor necrosis factor α (TNF-α). The survival rate after CA was decreased with time past. We found that histopathological score and TNF-α immunoreactivity were significantly increased in the lung after CA. These results indicate that inflammation triggered by ischemia-reperfusion damage after CA leads to pulmonary injury/dysfunctions and contributes to low survival rate. In addition, the finding of increase in TNF-α via inflammation in the lung after CA would be able to utilize therapeutic or diagnostic measures in the future.

KEYWORDS:

Asphyxial cardiac arrest; Lung; Post-cardiac arrest syndrome; Tumor necrosis factor α

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