Open AccessEffect of a neutrophil elastase inhibitor on acute lung injury after cardiopulmonary bypass
Author(s) -
Masahiro Fujii,
Yasuo Miyagi,
Ryuzo Bessho,
Takashi Nitta,
Masami Ochi,
Kazuo Shimizu
Publication year - 2010
Publication title -
interactive cardiovascular and thoracic surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.546
H-Index - 56
eISSN - 1569-9293
pISSN - 1569-9285
DOI - 10.1510/icvts.2009.225243
Subject(s) - medicine , cardiopulmonary bypass , neutrophil elastase , anesthesia , proinflammatory cytokine , cardiac surgery , elastase , cardiology , inflammation , biochemistry , chemistry , enzyme
Cardiopulmonary bypass (CPB) has been implicated as a cause of acute lung injury (ALI) in cardiac surgical patients. We used a bronchoscopic microsampling (BMS) probe to examine alveolar biochemical constituents and evaluated the effect of sivelestat sodium hydrate, a novel synthesized polymorphonuclear (PMN) neutrophil elastase inhibitor, on ALI induced by CPB. Twelve patients undergoing aortic valve replacement were treated with either sivelestat 0.2 mg/kg/h (sivelestat group, n=6) or 0.9% saline (control group, n=6) from the start of surgery. Samples were collected by the BMS probe at three time points: after tracheal intubation, 1 h after CPB introduction, and 3 h after CPB termination. Pulmonary function was assessed perioperatively. There were no differences in baseline characteristics. The concentration of PMN elastase was significantly suppressed in the sivelestat group, compared with the control group (P=0.001). The sivelestat group also had lower levels of interleukin-6 and interleukin-8. Alveolar-arterial oxygen difference markedly increased, and a worsening of the PaO(2)/FiO(2) ratio indicated severe impairment after CPB. However, sivelestat attenuated the pattern of physiological deterioration of gas exchange. Sivelestat may attenuate neutrophil elastase or proinflammatory cytokines, and improve pulmonary dysfunction in patients undergoing CPB.