Local and systemic impacts of pleural oxygen exposure in thoracotomy

Article type: Research Article

Authors: Tsukioka, Takuma^; | Takemura, Shigekazu | Minamiyama, Yukiko^; | Nishiyama, Noritoshi | Mizuguchi, Shinjiro | Okada, Shigeru | Suehiro, Shigefumi

Affiliations: Department of Cardiovascular Surgery, Osaka City University Graduate School of Medicine, Osaka, Japan | Department of Hepato-Biliary-Pancreatic Surgery, Osaka City University Graduate School of Medicine, Osaka, Japan | Department of Thoracic Surgery, Osaka City University Hospital, Osaka, Japan | Department of Anti-Aging Food Sciences, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University, Okayama, Japan

Note: [] Address for correspondence: Shigekazu Takemura, Department of Hepato-Biliary-Pancreatic Surgery, Osaka City University Graduate School of Medicine, 1-4-3 Asahimachi, Abeno-ku, Osaka 545-8585, Japan. Tel.: +81 6 6645 3841; Fax: +81 6 6646 6057; E-mail: [email protected]

Abstract: 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.

Keywords: Oxidative injury, pleural cavity, systemic inflammatory response, thoracic surgery

Journal: BioFactors, vol. 30, no. 2, pp. 117-128, 2007