Pulmonary vascular resistance and oxygenation index during EVLP.

<p>Pulmonary vascular resistance (A) was calculated as (mean pulmonary artery pressure - left atrial pressure)/perfusion flow). The oxygenation capacity (B) was calculated as the difference in the partial pressure of O₂ between the effluent and the affluent arms of the EVLP circuits. The vascular resistance and oxygenation capacity were computed after 60 minutes of EVLP (baseline values), and every 30 minutes thereafter. Means ± s.e.m. † p < 0.05 vs baseline value; * p<0.05 PDTC vs CTRL (two way ANOVA with Bonferroni’s adjustments for multiples comparisons).</p

Indices of lung edema.

<p>A. Weight gain of the heart-lung blocks expressed in grams, represents the difference between weight of the heart-lung blocks measured before and at the end of EVLP. B. The concentration of proteins in the BAL fluid (in mg^.ml^-1 BAL fluid) was measured as an index of high permeability edema. BASE: BAL fluid and was obtained from normal rats sacrificed without any intervention (Normal, baseline values, N = 3); CTRL: Ischemia followed by EVLP with Steen® solution alone (N = 6); PDTC: Ischemia followed by EVLP with PDTC treatment (N = 6). Means ± s.e.m.* p<0.05 (Heart-lung block weight gain: unpaired <i>t</i> test; Proteins in BAL fluid: ANOVA followed by Tukey’s test).</p

Static pulmonary compliance and peak airway pressure during EVLP.

<p>Static pulmonary compliance (A) and peak airway pressure (B) were computed 60 minutes after EVLP initiation (baseline values), and every 30 minutes thereafter. CTRL: Ischemia followed by EVLP with Steen® solution alone (N = 6); PDTC: Ischemia followed by EVLP with PDTC treatment (N = 6). Means ± s.e.m. † p < 0.05 vs baseline value; * p<0.05 PDTC vs CTRL (two way ANOVA with Bonferroni’s adjustments for multiples comparisons)</p

LDH activity in BAL fluid and protein carbonyls in lung tissue homogenates.

<p>A. LDH activity in BAL fluid. LDH activity was measured as an index of cellular necrosis, expressed in arbitrary units (A.U.). B: protein carbonyls were measured as an index of oxidative modifications in lung tissue, normalized to the concentration of lung proteins. BASE: BAL fluid and lung tissue were obtained from normal rats sacrificed without any intervention (Normal, baseline values, N = 3); CTRL: Ischemia followed by EVLP with Steen® solution alone (N = 6); PDTC: Ischemia followed by EVLP with PDTC treatment (N = 6). Means ± s.e.m.* p<0.05 (ANOVA followed by Tukey’s test).</p

Concentrations of inflammatory cytokines in the BAL fluid.

<p>BAL fluid concentration of IL-6 (A), TNFα (B) and CINC-1 (C), expressed in ng^.ml^-1 BAL fluid. BASE group: BAL fluid was obtained from normal rats sacrificed without any intervention (normal values, N = 3); CTRL: Ischemia followed by EVLP with Steen® solution alone (N = 6); PDTC: Ischemia followed by EVLP with PDTC treatment (N = 6). Means ± s.e.m.* p<0.05. (ANOVA followed by Tukey’s test).</p

Experimental protocol.

<p>Rats were sacrificed by exsanguination and perfusion cannulae were inserted into the pulmonary artery and the left atrium. The chest was left open for one hour at room temperature (warm ischemic time), with the lungs deflated. The lungs were then flushed with cold Perfadex® solution, inflated (5ml·kg^-1, FiO₂ 0.5), and kept 2 hours in 4°C Perfadex® (cold ischemic time). The heart-lung blocks were then weighted (lung weight 1) mounted into a rat EVLP system, and perfused for a total of 4 hours, either with Steen® solution alone (Control group, CTRL, N = 6) or with Steen® solution supplemented with pyrrolidine dithiocarbamate ammonium (PDTC, C₅H₉NS₂-NH₃), at a concentration of 2.5g·L^-1 (PDTC group, N = 6). At the end of EVLP protocol, the heart-lung blocks were once again weighted (lung weight 2), a bronchoalveolar lavage was performed through the tracheal cannula, and the left lung was frozen for further analysis.</p