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Ann Thorac Surg 1993;56:0003497593906747
© 1993 The Society of Thoracic Surgeons

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Articles

Endothelium-dependent relaxation in pulmonary arteries after lung preservation and transplantation

Department of Cardiothoracic Surgery, University Hospital, Lund, Sweden

Accepted for publication January 22, 1993.

^_* Address reprint requests to Dr Steen, Department of Cardiothoracic Surgery, University Hospital of Lund, S-221 85 Lund, Sweden.

Pulmonary hypertension is frequently seen after lung transplantation. To study how the release of the endothelium-dependent relaxing factor is affected by lung preservation and transplantation, porcine pulmonary arteries were investigated in organ baths. The arteries (1 mm in diameter) were taken from fresh nonperfused lungs (group I), lungs immediately after flush-perfusion with a low-potassium-dextran solution (group II), non-perfused lungs stored for 12 hours in low-potassium-dextran solution (group III), flush-perfused lungs stored for 12 hours in low-potassium-dextran solution (group IV), and group IV lungs after left lung transplantation and right pneumonectomy followed by 24 hours of reperfusion (group V). Stable contractions were induced with the thromboxane A₂ analogue U-46619. Acetylcholine was used to stimulate the release of endothelium-dependent relaxing factor. In vessel segments where the endothelium had been removed, acetylcholine elicited no response. In segments with intact endothelium, acetylcholine induced concentration-dependent relaxation; the maximum relaxation obtained was 91% ± 3% (I), 86% ± 3% (II), 85% ± 3% (III), 69% ± 5% (IV), and 69% ± 9% (V). Relaxation was significantly reduced in groups IV (p < 0.01) and V (p < 0.05) as compared with group I. Stable moderate pulmonary hypertension was present in all the transplanted lungs throughout the 24-hour observation period. It is concluded that the endothelium-mediated relaxation is significantly reduced after flush perfusion combined with 12 hours of storage in low-potassium-dextran solution. Lung transplantation, followed by 24 hours of reperfusion did not further impair the endothelium-dependent relaxation.