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Cold ischemia and reperfusion each produce pulmonary vasomotor dysfunction in the transplanted lung.

Authors
  • Fullerton, D A
  • Mitchell, M B
  • McIntyre, R C Jr
  • Banerjee, A
  • Campbell, D N
  • Harken, A H
  • Grover, F L
Type
Published Article
Journal
Journal of Thoracic and Cardiovascular Surgery
Publisher
American Association for Thoracic Surgery
Publication Date
Dec 01, 1993
Volume
106
Issue
6
Pages
1213–1217
Identifiers
PMID: 8246563
Source
Medline
License
Unknown

Abstract

Pulmonary vascular resistance is significantly increased in the transplanted lung. We hypothesized that the ischemic or reperfusion injuries incurred by the transplanted lung may produce pulmonary vasomotor dysfunction, which in turn may produce increased pulmonary vascular resistance. In a dog model of autologous lung transplantation, the purpose of this study was to examine the following mechanisms of pulmonary vasomotor control and to relate each of them to cold ischemia and to reperfusion: (1) endothelium-dependent cyclic guanosine monophosphate-mediated vasorelaxation (response to acetylcholine 10(-6) mol/L), (2) endothelium-independent cyclic guanosine monophosphate-mediated vasorelaxation (response to sodium nitroprusside 10(-6) mol/L), and beta-adrenergic cyclic adenosine monophosphate-mediated vasorelaxation (response to isoproterenol 10(-6) mol/L). Autologous right lung transplantation was performed in five dogs. At each of three times, two third-order pulmonary arteries were dissected from each transplanted lung and studied: control (immediately after harvest), cold ischemia (3 hours in 4 degrees C saline solution), and cold ischemia plus reperfusion (1 hour after lung reimplantation). The vasorelaxing effects of acetylcholine, sodium nitroprusside, and isoproterenol were studied in isolated pulmonary arterial rings, suspended on fine wire tensiometers in individual organ chambers. Statistical analysis was by analysis of variance. Results demonstrated significant dysfunction of beta-adrenergic cyclic adenosine monophosphate-mediated relaxation after cold ischemia alone, and this dysfunction was exacerbated by reperfusion. Endothelium-dependent cyclic guanosine monophosphate-mediated relaxation was not impaired by cold ischemia alone but was significantly impaired by reperfusion. Endothelium-independent cyclic guanosine monophosphate-mediated relaxation was not impaired by cold ischemia or reperfusion. We conclude that cold ischemia and reperfusion each produce different patterns of pulmonary vasomotor dysfunction. Cumulatively, such dysfunction may contribute to increased pulmonary vascular resistance in the transplanted lung.

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