Lung transplant reperfusion injury involves pulmonary macrophages and circulating leukocytes in a biphasic response

Citation
Sm. Fiser et al., Lung transplant reperfusion injury involves pulmonary macrophages and circulating leukocytes in a biphasic response, J THOR SURG, 121(6), 2001, pp. 1069-1075
Citations number
22
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY
ISSN journal
00225223 → ACNP
Volume
121
Issue
6
Year of publication
2001
Pages
1069 - 1075
Database
ISI
SICI code
0022-5223(200106)121:6<1069:LTRIIP>2.0.ZU;2-#
Abstract
Objective: Both donor pulmonary macrophages and recipient circulating leuko cytes may be involved in reperfusion injury after lung transplantation. By using the macrophage inhibitor gadolinium chloride and leukocyte filters, w e attempted to identify the roles of these two populations of cells in lung transplant reperfusion injury. Methods: With our isolated, ventilated, blood-perfused rabbit lung model, a ll groups underwent lung harvest followed by 18-hour cold storage and 2-hou r blood reperfusion. Measurements of pulmonary artery pressure, lung compli ance, and arterial oxygenation were obtained. Group I (n = 8) served as a c ontrol. Group IT (n = 8) received gadolinium chloride at 14 mg/kg 24 hours before lung harvest. Group III (n = 8) received leukocyte-depleted blood re perfusion by means of a leukocyte filter. Results: The gadolinium chloride group had significantly improved arterial oxygenation and pulmonary artery pressure measurements compared with contro l subjects and an improved arterial oxygenation compared with the filter gr oup after 30 minutes of reperfusion. After 120 minutes of reperfusion, howe ver, the filter group had significantly improved arterial oxygenation and p ulmonary artery pressure measurements compared with the control group and a n improved arterial oxygenation compared with the gadolinium chloride group . Conclusions: Lung transplant reperfusion injury occurs in two phases. The e arly phase is mediated by donor pulmonary macrophages and is followed by a late injury induced by recipient circulating leukocytes.