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Postmortem and ex vivo carbon monoxide ventilation reduces injury in rat lungs transplanted from non–heart-beating donors  Boming Dong, MD, PhD, Paul.

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Presentation on theme: "Postmortem and ex vivo carbon monoxide ventilation reduces injury in rat lungs transplanted from non–heart-beating donors  Boming Dong, MD, PhD, Paul."— Presentation transcript:

1 Postmortem and ex vivo carbon monoxide ventilation reduces injury in rat lungs transplanted from non–heart-beating donors  Boming Dong, MD, PhD, Paul W. Stewart, PhD, Thomas M. Egan, MD, MSc  The Journal of Thoracic and Cardiovascular Surgery  Volume 146, Issue 2, Pages e1 (August 2013) DOI: /j.jtcvs Copyright © 2013 The American Association for Thoracic Surgery Terms and Conditions

2 Figure 1 Effect of carbon monoxide (CO) ventilation on pulmonary function. A, After perfusion in the circuit, donor lungs ventilated with 500 ppm CO/60% oxygen (CO-vent) developed less edema than controls (Ctrl), which were ventilated with 60% oxygen (∗P = .036). One hour after lung transplant, the mean wet-to-dry weight ratio was similar in CO-vent and control lungs. B, After transplant, oxygenation in CO-ventilated graft lungs was better than in control lungs (†P = .0058). C, Flow to the graft lung (L) expressed as a ratio to total flow [LPA = (LPA flow rate/donor weight)/(PA flow rate/recipient weight)] was similar in the 2 groups (P = .14). The mean ± 1 standard error is shown for control lungs (n = 6) and CO-vent (n = 6). R, Right; Recip, recipient; PaO2/FiO2, measured arterial pO2/fractional inhaled oxygen concentration; LPV, left pulmonary vein; LPA, left pulmonary artery; PA, pulmonary artery. The Journal of Thoracic and Cardiovascular Surgery  , e1DOI: ( /j.jtcvs ) Copyright © 2013 The American Association for Thoracic Surgery Terms and Conditions

3 Figure 2 Lung tissue cyclic guanosine monophosphate (cGMP). Mean cGMP levels in transplanted lungs was increased in the carbon monoxide–ventilated (CO-vent) group 1 hour after lung transplantation (∗P = .0358). The mean ± 1 standard error is shown for controls (n = 5) and CO-vent (n = 6). The Journal of Thoracic and Cardiovascular Surgery  , e1DOI: ( /j.jtcvs ) Copyright © 2013 The American Association for Thoracic Surgery Terms and Conditions

4 Figure 3 Western blots for nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα) and mitogen-activated protein kinases (MAPKs). Each graph is shown with a representative blot. A, IκBα was degraded in both carbon monoxide–ventilated (CO-vent) (n = 5) and control (n = 6) transplanted lungs, but less degradation was observed in the CO-vent group (∗P = .0098). B, p38 Activation was noted in the CO-vent (n = 6) and control (n = 5) groups but was more pronounced in the CO-vent group (†P =.0032). C, c-Jun N-terminal kinase (JNK) activation was also observed in both groups (n = 5 per group) and was reduced by the CO-vent treatment (†P = .0077). D, Extracellular signal-regulated kinase (ERK) activation was observed in the CO-vent (n = 5) and control (n = 6) groups. The mean ± 1 standard error is shown for each group. The Journal of Thoracic and Cardiovascular Surgery  , e1DOI: ( /j.jtcvs ) Copyright © 2013 The American Association for Thoracic Surgery Terms and Conditions

5 Figure 4 Reverse transcription-polymerase chain reaction (RT-PCR) for genes indicated. One hour after transplant, carbon monoxide ventilation (CO-vent) was associated with increased upregulation of heme oxygenase-1 (HO-1+) (∗P = .0314) (A), decreased upregulation of IL-6 (∗P = .0192, n = 5 per group) (B), and decreased upregulation of interleukin 1-beta (IL-1β) (∗P = .0262, n = 6 per group) (C). The 2 treatment groups were similar in regard to upregulation of tumor necrosis factor-alpha (TNF-α) (P = .087) (D), upregulation of intercellular adhesion molecule-1 (ICAM-1) (P = .99) (E), and downregulation of endothelial nitric oxide synthase (eNOS) (P = .75, n = 5 CO-vent and n = 6 controls) (F). For each of A through F, for at least 1 of the 2 treatments, the post–lung transplant mean was statistically significantly different from the mean for fresh tissue samples. The Journal of Thoracic and Cardiovascular Surgery  , e1DOI: ( /j.jtcvs ) Copyright © 2013 The American Association for Thoracic Surgery Terms and Conditions

6 Figure 5 Scatter plot of log10-transformed interleukin-6 (IL-6) and interleukin-1 beta (IL-1β) messenger RNA pairs from carbon monoxide–ventilated (squares) and control (circles) post-transplant lung samples. Near-perfect correlation (r2 = 0.98) suggests that the signaling pathway(s) responsible for upregulation of IL-6 and IL-1β post-transplant are likely identical and equally inhibited by CO-ventilation. The Journal of Thoracic and Cardiovascular Surgery  , e1DOI: ( /j.jtcvs ) Copyright © 2013 The American Association for Thoracic Surgery Terms and Conditions

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