Superoxide anion mediates pulmonary vascular permeability caused by neutrophils in cardiopulmonary bypass

Tatsuo Tanita, Chun Song, Hiroshi Kubo, Yasushi Hoshikawa, Masayuki Chida, Satoshi Suzuki, Sadafumi Ono, Shigefumi Fujimura

研究成果: ジャーナルへの寄稿学術論文査読

15 被引用数 (Scopus)

抄録

During cardiopulmonary bypass (CPB), neutrophils (PMNs) may be stimulated by shear stress which could contribute to the pulmonary injury that occurs after CPB. To elucidate whether mechanically stimulated PMNs increase pulmonary vascular permeability, measured as the pulmonary filtration coefficient (K) and pulmonary vascular resistance, and to elucidate whether superoxide anion mediates this increase, we assessed the effects of stimulated and unstimulated PMNs, and of superoxide dismutase (SOD) on K and resistance in isolated perfused lungs from Sprague-Dawley rats. PMNs were stimulated by gentle agitation in a glass vial for 10s. Lungs perfused with the stimulated PMNs, being the stimulated group (n = 6), elicited a 5-fold increase in the filtration coefficient compared with lungs perfused with unstimulated cells, being the unstimulated group (n = 6). This increase in filtration was completely blocked by the preincubation of stimulated PMNs with CD18 monoclonal anti-body, being the Ab group (n = 6), and also by superoxide dismutase, being the SOD group (n = 6). Pulmonary vascular resistance was not increased by stimulated PMNs, and the accumulation of stimulated PMNs was not blocked by SOD. These findings suggest that stimulated PMNs increase K and that superoxide anion may injure the pulmonary vascular endothelial cells.

本文言語英語
ページ(範囲)755-761
ページ数7
ジャーナルSurgery Today
29
8
DOI
出版ステータス出版済み - 1999
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All Science Journal Classification (ASJC) codes

  • 外科

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