Institutions where work was performed: Australian Red Cross Blood Service, Brisbane, Qld, Australia The Critical Care Research Group, The Prince Charles Hospital, Brisbane, Qld, Australia Medical Engineering Research Facility, Queensland University of Technology, Brisbane, Qld, Australia.
A novel in vivo ovine model of transfusion-related acute lung injury (TRALI)
Article first published online: 26 JUL 2010
© 2010 The Author(s). Vox Sanguinis © 2010 International Society of Blood Transfusion
Volume 100, Issue 2, pages 219–230, February 2011
How to Cite
Tung, J. P., Fung, Y. L., Nataatmadja, M., Colebourne, K. I., Esmaeel, H. M., Wilson, K., Barnett, A. G., Wood, P., Silliman, C. C. and Fraser, J. F. (2011), A novel in vivo ovine model of transfusion-related acute lung injury (TRALI). Vox Sanguinis, 100: 219–230. doi: 10.1111/j.1423-0410.2010.01381.x
- Issue published online: 11 JAN 2011
- Article first published online: 26 JUL 2010
- Received: 13 May 2010, revised 5 July 2010, accepted 5 July 2010, published online 26 July 2010
- animal models;
Background and Objectives Even with the introduction of specific risk-reduction strategies, transfusion-related acute lung injury (TRALI) continues to be a leading cause of transfusion-related morbidity and mortality. Existing small animal models have not yet investigated TRALI resulting from the infusion of heat-treated supernatant from whole blood platelet concentrates. In this study, our objective was the development of a novel in vivo two-event model of TRALI in sheep.
Materials and Methods Lipopolysaccharide (LPS; 15 μg/kg) as a first event, modelled clinical infection. Transfusion (estimated at 10% of total blood volume) of heat-treated pooled supernatant from date-of-expiry human whole blood platelet concentrates (d5-PLT-S/N) was used as a second event. TRALI was defined by both hypoxaemia that developed either during the transfusion or within two hours of its completion and post-mortem histological evidence of pulmonary oedema.
Results LPS infusion did not cause lung injury itself, but did result in decreased circulating levels of lymphocytes and neutrophils with evidence of the latter becoming sequestered in the lungs. Sheep that received LPS (first event) followed by d5-PLT-S/N (second event) displayed decreased pulmonary compliance, decreased end tidal CO2 and increased arterial partial pressure of CO2 relative to control sheep, and 80% of these sheep developed TRALI.
Conclusions This novel ovine two-event TRALI model presents a new tool for the investigation of TRALI pathogenesis. It represents the first description of an in vivo large animal model of TRALI and the first description of TRALI caused by transfusion with heat-treated pooled supernatant from human whole blood platelet concentrates.