Document Detail


Cold ischemia and reperfusion each produce pulmonary vasomotor dysfunction in the transplanted lung.
MedLine Citation:
PMID:  8246563     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
D A Fullerton; M B Mitchell; R C McIntyre; A Banerjee; D N Campbell; A H Harken; F L Grover
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  The Journal of thoracic and cardiovascular surgery     Volume:  106     ISSN:  0022-5223     ISO Abbreviation:  J. Thorac. Cardiovasc. Surg.     Publication Date:  1993 Dec 
Date Detail:
Created Date:  1994-01-04     Completed Date:  1994-01-04     Revised Date:  2003-11-14    
Medline Journal Info:
Nlm Unique ID:  0376343     Medline TA:  J Thorac Cardiovasc Surg     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1213-7     Citation Subset:  AIM; IM    
Affiliation:
University of Colorado Health Sciences Center, Denver 80262.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cyclic AMP / physiology
Cyclic GMP / physiology
Dogs
Ischemia / physiopathology*
Lung / blood supply*,  physiopathology*
Lung Transplantation / adverse effects,  physiology*
Muscle, Smooth, Vascular / physiology
Reperfusion Injury / physiopathology*
Vascular Resistance / physiology
Vasomotor System / physiology*
Chemical
Reg. No./Substance:
60-92-4/Cyclic AMP; 7665-99-8/Cyclic GMP

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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