Pulmonary vascular resistance related to endothelial function after lung transplantation

Abstract

In 8 donor pigs, flush perfusion was performed with a low-potassium-dextran solution. Ring segments were taken from a smalt intralobar pulmonary artery in the right lung immediately after perfusion and after 24 hours of cold storage for studies in organ baths. Stable vasoconstriction was induced with the thromboxane mimic U-46619, and acelylcholine was used to induce endothelium-dependent relaxation. The maximum relaxation was significantly reduced after flush perfusion compared with fresh nonperfused controls, and a significant additional reduction was seen after the 24-hour storage period. The left donor lung was transplanted into a recipient after 24 hours of cold storage. Contralateral pneumonectomy was then performed, making the recipient entirely dependent on the transplanted lung for survival. All 8 pigs were in good condition throughout the 24-hour observation period, with arterial oxygen tension of around 165 mm Hg (range, 80 to 275 mm Hg; inspired oxygen fraction, 0.5) and pulmonary vascular resistance of around 450 dyne · s · cm −5 (range, 260 to 730 dyne · s · cm −5). The maximum endothelium-dependent relaxation for each donor was checked for correlation (to pulmonary vascular resistance and to systolic, mean, and diaslolic pulmonary artery pressures as recorded at 4-hour intervals. Regression analyses showed arterial oxygen tension to be unrelated to pulmonary vascular resistance and endothelial dysfunction to be unrelated to pulmonary artery pressure but to correlate to pulmonary vascular resistance, this correlation being significant after reperfusicn for 16 hours ( p < 0.05) and highly significant after 24 hours ( p < 0.001). Thus, endothelial dysfunction appears to contribute to the increase in pulmonary vascular resistance after transplantation.