Fujii 2010.

Study characteristics
Methods	Prospective, randomised study Run‐in period: not specified; received 8 October 2009; received in revised form 17 February 2010; accepted 3 March 2010 Number of study centres and locations: single centre; Division of Cardiovascular Surgery, Department of Surgery, Nippon Medical School Hospital (Tokyo, Japan)
Participants	Twelve participants were treated with either sivelestat 0.2 mg/kg/h (sivelestat group, n = 6) or 0.9% saline (control group, n = 6). Mean age: 70.75 years Sex (female/male ratio): 66.67% No high‐risk population Inclusion criteria: > 20 years of age and scheduled to undergo elective AVR surgery Exclusion criteria: presence of cardiogenic pulmonary oedema, emergency or urgent cases, pre‐existing asthma or COPD, and major chest wall abnormalities
Interventions	Intervention group: sivelestat sodium hydrate, a novel synthesised PMN‐Elastase inhibitor (dissolved in 50 mL of 5% glucose solution and administered intravenously at a rate of 0.2 mg/kg/h for 24 hours as a continuous infusion after tracheal intubation) Control group: 0.9% saline from the start of surgery
Outcomes	Clinical parameters (mortality, major complications, reoperation, time to extubation), pulmonary function (AaDO2, PaO2/FiO2 ratio), IL‐6 and IL‐8, and PMN‐Elastase Timing: after tracheal intubation, 1 hour after CPB introduction, and 3 hours after CPB termination. Data were drawn from plasma and trough bronchoscopic microsampling procedure.
Notes
Risk of bias
Bias	Authors' judgement	Support for judgement
Random sequence generation (selection bias)	Low risk	There were no differences in baseline characteristics. Patients were randomised into two groups using a computer‐generated randomisation table.
Allocation concealment (selection bias)	Unclear risk	The drug administration was blinded for the surgical and anaesthesiologic teams, but there was no further description of how allocation was made.
Blinding of participants and personnel (performance bias) All outcomes	Low risk	Surgical and anaesthesiologic teams were blinded. All determinations of cytokines in the alveolar biochemical constituents were carried out by a technician blinded to treatment allocation.
Blinding of outcome assessment (detection bias) All outcomes	Low risk	All determinations of cytokines in the alveolar biochemical constituents were carried out by a technician blinded to treatment allocation.
Incomplete outcome data (attrition bias) All outcomes	Low risk	All participants survived and completed the study, with no trial group changes, no withdrawals, and no losses to follow‐up reported but with no ITT analysis. Data from all participants were included in the final analysis.
Selective reporting (reporting bias)	Unclear risk	Inflammatory marker data were detected only from the alveolar biochemical constituents. They are not clearly reported in the Results section of the paper.
Other bias	Low risk	No funding was disclosed.