LUNG TRANSPLANTATION WITH CARDIOPULMONARY BYPASS EXAGGERATES PULMONARY VASOMOTOR DYSFUNCTION IN THE TRANSPLANTED LUNG

Pulmonary vascular resistance is significantly increased in the transp lanted lung, If cardiopulmonary bypass is required, the transplanted l ung is reperfused with activated blood elements, which might exacerbat e the reperfusion injury, The purpose of this study was to examine the influence of cardiopulmonary bypass on the following mechanisms of pu lmonary vasomotor control in a dog model of autologous lung transplant ation: (1) endothelium-dependent cyclic guanosine monophosphate-mediat ed relaxation (response to acetylcholine), (2) endothelium-independent cyclic guanosine monophosphate-mediated relaxation (response to nitro prusside), and (3) beta-adrenergic cyclic adenosine monophosphate-medi ated relaxation (response to isoproterenol). Autologous right lung tra nsplants were performed with (n = 4 dogs) and without (n = 5 dogs) byp ass. Lungs were stored in cold saline solution (4 degrees C, 3 hours) before reimplantation. Pulmonary vasomotor control mechanisms were stu died in isolated pulmonary arterial rings immediately after harvest an d 1 hour after reimplantation. Ten rings were studied in each group at each time. Statistical analysis was by analysis of variance. Without bypass, endothelium-dependent cyclic guanosine monophosphate-mediated relaxation and beta-adrenergic cyclic adenosine monophosphate-mediated relaxation were significantly impaired, although endothelium-independ ent cyclic guanosine monophosphate-mediated relaxation was not. Use of bypass produced significantly greater impairment of both endothelium- dependent cyclic guanosine monophosphate-mediated relaxation and beta- adrenergic cyclic adenosine monophosphate-mediated relaxation. In addi tion, use of bypass produced significant dysfunction of endothelium-in dependent cyclic guanosine monophosphate-mediated relaxation as well. We conclude that using cardiopulmonary bypass to perform lung transpla ntation greatly exaggerates pulmonary vasomotor dysfunction in the tra nsplanted lung. This dysfunction may contribute to significantly highe r pulmonary vascular resistance in the transplanted lung if cardiopulm onary bypass is used.