Objective: To evaluate the effects of prearrest heparin administration on lung quality in a model of donation after cardiac death (DCD), and to assess the potential application of ex vivo lung perfusion (EVLP) in the identification of better grafts from the DCD donor pool.
Methods: Cardiac death was induced by electric shock in 10 pigs. One group received a prearrest heparin dose of 300 units/kg (H group, n = 5) and the other did not (NH group, n = 5). Animals remained at room temperature for 1 hour without ventilation, defining the warm ischemic time. After harvest, the lungs underwent 6 hours of cold ischemia before being evaluated with EVLP for 4 hours.
Results: Static compliance 28 ± 3 versus 29 ± 2 (Cstat—cm H2O), pulmonary vascular resistance (PVR) 593 ± 127 versus 495 ± 70 (PVR—dyn·s/cm5), and oxygenation 327 ± 32 versus 330 ± 28 (ΔPO2—mm Hg) remained stable from the beginning until the end of EVLP in the H group. In the NH group, Cstat started to decline after the first hour (25 ± 2 vs 21 ± 2), ΔPO2 after hour 2 (265 ± 44 vs 207 ± 44), and PVR started to increase after hour 3 (765 ± 132 vs 916 ± 168). Significant differences between the groups were observed at the end of EVLP (P < 0.001). Parameters of lung quality after EVLP also showed significant differences between the groups: wet weight-to-dry weight ratio (P < 0.001), protein in the bronchial lavage (P < 0.01), Na+ + K+-ATPase activity (P < 0.001), and E-selectin (P < 0.001) in the perfusate.
Conclusions: Prearrest heparin administration improved organ function by preserving endothelial homeostasis. EVLP proved to be a useful platform for assessing DCD lungs, providing reliable means of discriminating injured grafts.
This report evaluated the effects of prearrest heparinization in a swine model of donation after cardiac death. The group that did not receive heparin presented platelet activation, endothelial inflammation, and thrombi formation; these effects led to early organ failure during ex vivo lung perfusion.
From the Artificial Organs Laboratory, Division of Cardiac Surgery, University of Maryland School of Medicine, Baltimore, MD.
Reprints: Bartley P. Griffith, MD, Division of Cardiac Surgery, 22 S. Greene St, Room N4W96, Baltimore, MD 21201. E-mail: firstname.lastname@example.org.
Disclosure: This study was partially supported by an educational grant provided by XVIVO (Goteborg, Sweden) to the University of Maryland School of Medicine.