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Trigger for intercellular adhesion molecule-1 expression in rat lungs transplanted from non-heart-beating donors
Thomas M Egan1, Yalaunda Thomas, Debra Gibson
1University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA. ltxtme@med.unc.edu
The Annals of Thoracic Surgery
|March 3, 2004
Summary
Reperfusion, not ischemia, triggers intercellular adhesion molecule-1 (ICAM-1) upregulation in lung transplants. Strategies targeting reperfusion may reduce ICAM-1 expression and injury in lung grafts.
Area of Science:
- Transplantation immunology
- Organ preservation and transplantation
Background:
- Lung transplantation from non-heart-beating donors is associated with ischemia-reperfusion injury.
- Intercellular adhesion molecule-1 (ICAM-1) is implicated in inflammatory responses following organ transplantation.
Purpose of the Study:
- To identify the specific trigger for intercellular adhesion molecule-1 (ICAM-1) expression during ischemia-reperfusion injury in lung transplantation.
- To differentiate the roles of ischemia versus reperfusion in initiating ICAM-1 upregulation.
Main Methods:
- Rat left lung transplants were performed using lungs from non-heart-beating donors with varying ventilation and reperfusion times.
- Immunohistochemical staining for ICAM-1 was conducted on lung tissues.
- Expression levels of ICAM-1 were graded by masked observers and compared statistically.
Main Results:
- Constitutive ICAM-1 expression was observed in normal rat lung alveoli.
- No significant increase in ICAM-1 expression was found at 4 hours of reperfusion, regardless of donor type.
- A significant increase in ICAM-1 expression in alveolar and arteriolar areas was noted at 6 hours of reperfusion in lungs from non-heart-beating donors.
Conclusions:
- The onset of reperfusion, rather than ischemia or total ischemic time, is the primary signal for ICAM-1 upregulation in lung transplants.
- Interventions aimed at the reperfusion phase may be crucial for mitigating ICAM-1 expression and subsequent injury.
- Lung transplantation immediately after circulatory arrest does not induce sufficient injury to upregulate ICAM-1.