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Intratracheal Antitumor Necrosis Factor‐α Antibody Attenuates Lung Tissue Damage Following Cardiopulmonary Bypass
Author(s) -
Qi Danni,
Gao MingXin,
Yu Yang
Publication year - 2013
Publication title -
artificial organs
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.684
H-Index - 76
eISSN - 1525-1594
pISSN - 0160-564X
DOI - 10.1111/j.1525-1594.2012.01542.x
Subject(s) - cardiopulmonary bypass , tumor necrosis factor alpha , medicine , lung , malondialdehyde , saline , apoptosis , mechanical ventilation , pharmacology , pulmonary injury , necrosis , anesthesia , immunology , chemistry , oxidative stress , pulmonary fibrosis , biochemistry
The aim of this study is to investigate the protective effect and underlying mechanism of antitumor necrosis factor‐α antibody (TNF‐α Ab) on lung tissue injury after cardiopulmonary bypass (CPB). Twenty‐eight healthy New Zealand white rabbits were randomly divided into four groups. Group I received only an open chest operation. Groups II–IV all received CPB. Furthermore, groups III and IV received post‐CPB endotracheal intubation with phosphate buffered saline or TNF‐α Ab (2400 pg/kg), respectively. Perioperative blood neutrophil count, TNF‐α level, and malondialdehyde (MDA) levels were determined in both the right and left atriums. Lung water content, TNF‐α messenger RNA, protein, apoptosis in situ, and pathomorphological changes were also measured. The results show that TNF‐α Ab can significantly inhibit leukocyte accumulation, reduce secretion of TNF‐α and MDA, decrease lung tissue apoptosis, and attenuate post‐CPB pathomorphological changes. TNF‐α Ab administration, however, cannot suppress the expression of TNF‐α, suggesting that the protective effects of TNF‐α Ab originate from inhibiting the numerous biological functions of TNF‐α. Intratracheal TNF‐α Ab administration demonstrates a notable protective effect against lung injury after CPB.