ABSTRACT
BACKGROUND: Our previous study showed that retrograde flush through the left atrium is better than antegrade flush in 6-hour lung preservation. Whether it is feasible in long-term lung preservation is not clear. Several studies suggested that prostaglandin E1 may not be necessary in retrograde flush because of the low vascular resistance on the venous side. This study evaluates the effects of retrograde flush and prostaglandin E1 in 24-hour lung preservation. METHODS: Canine donor lungs were retrograde flushed with University of Wisconsin solution. Group A (n = 7) was pretreated with prostaglandin E1. No prostaglandin E1 was used in group B (n = 7). After flush and cold storage at 4 degrees C for 22 to 25 hours, left lung allotransplantation was performed. Measurements were taken before transplantation (baseline), and at 10, 30, 60, and 120 minutes after transplantation while the right pulmonary artery was occluded. RESULTS: After 120 minutes of reperfusion, the oxygen tension and carbon dioxide tension were 643 +/- 24 and 37 +/- 3 mm Hg in group A and 600 +/- 29 and 37 +/- 3 mm Hg in group B, respectively (p = NS). Pulmonary artery pressure (group A vs group B) was 20 +/- 1 versus 28 +/- 2 mm Hg (p < 0.01); right atrium pressure: 4 +/- 1 versus 8 +/- 1 mm Hg (p < 0.01); left pulmonary vascular resistance: 1109 +/- 51 versus 1525 +/- 133 dyne.sec.cm-5 (p < 0.05); airway resistance: 22 +/- 1 versus 24 +/- 1 cm H2O/L/sec (p = NS); lung dynamic compliance: 30 +/- 1 versus 26 +/- 1 cc/cm (p < 0.05) respectively. As compared with the baseline (19 +/- 1), airway resistance was significantly increased after 2 hours of reperfusion in group B (p < 0.05). Electron microscopy revealed that type I pneumocytes, capillary endothelial cells, and epithelial cells of bronchi were well preserved and the contents of lamellar bodies of type II pneumocyte were reduced. CONCLUSIONS: Canine lung was well preserved by retrograde flush and cold storage with University of Wisconsin solution after 24 hours preservation. Pretreatment of prostaglandin E1 is helpful in reducing pulmonary vascular resistance and airway resistance and improving lung dynamic compliance.
