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Local and systemic impacts of pleural oxygen exposure in thoracotomy
Author(s) -
Tsukioka Takuma,
Takemura Shigekazu,
Minamiyama Yukiko,
Nishiyama Noritoshi,
Mizuguchi Shinjiro,
Okada Shigeru,
Suehiro Shigefumi
Publication year - 2007
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.5520300205
Subject(s) - thoracotomy , medicine , business , intensive care medicine , cardiology
The pleural cavity is normally in a state of negative pressure and low oxygen tension. It is exposed to the atmosphere during thoracic surgery. However, no reports of pathophysiological investigation of the effects of pleural oxygen exposure involved in thoracotomy are available. In this study, the effects of pleural oxygen exposure on systemic and pleural inflammation were investigated. Male Wistar rats (9 weeks old) were placed on mechanical ventilation and underwent thoracotomy with lipopolysaccharide (LPS) administration, which simulates latent inflammatory condition. The pleural cavity was exposed to nitrogen (N 2 thoracotomy group), air (20% oxygen, air thoracotomy group), or 100% oxygen (O 2 thoracotomy group) under mechanical ventilation for 2 h. Animals were sacrificed 2 h or 8 h after LPS administration, and inflammatory indices (plasma tumor necrosis factor‐α and interleukin‐6, histology) were examined. For examination of inflammatory mediators, pleural effusion was added to cultured RAW264 cells, a murine macrophage cell line, and tumor necrosis factor‐α levels in supernatant were measured. The capacity of pleural superoxide generation was investigated without LPS administration. Results showed increases in plasma interleukin‐6 concentration and lung injury in the air and O 2 thoracotomy groups. Pleural oxygen exposure stimulated pleural superoxide generation, and increased pleural 4‐hydroxy–2‐nonenal and lung lipid peroxide concentrations. Tumor necrosis factor‐α levels in cell culture supernatants were increased by the addition of pleural effusion from the air and O 2 thoracotomy groups. In conclusion, pleural oxygen exposure induced pleural oxidative injury and aggravated latent systemic inflammatory response.