Experimental interventions that reduce ischaemia/reperfusion (I/R) lung injury can be used to improve the properties of preservation solutions. We attempted to increase the attenuation of I/R injury by University of Wisconsin solution (UW) by adding an antibody against tumour necrosis factor-α (TNF-α), to neutralize TNF-α, and/or by adding 3-deaza-adenosine (c3-Ado), to inhibit leucocyte adhesion and the biosynthesis of ICAM-1 (intercellular cell-adhesion molecule 1). We examined I/R injury using an isolated rat lung model. Six different solutions were perfused individually, followed by evaluation of I/R injury: (1) 0.9% NaCl (normal saline; NS), (2) NS+anti-TNF-α antibody, (3) UW alone, (4) UW+anti-TNF-α, (5) UW+c3-Ado and (6) UW+anti-TNF-α+c3-Ado. Haemodynamic changes, lung weight gain, capillary filtration coefficient, TNF-α levels and lung pathology were analysed in order to evaluate I/R injury. Compared with lungs perfused with NS, lungs treated with NS+anti-TNF-α showed less I/R injury. The addition of anti-TNF-α and/or c3-Ado to UW reduced I/R injury compared with unmodified UW. Among the six solutions tested, UW containing anti-TNF-α antibody reduced I/R injury to the greatest extent. We conclude that addition of anti-TNF-α antibody or c3-Ado protects against I/R lung injury when using UW. Further investigation of the improved properties of modified UWs would be beneficial with regard to lung transplantation research.
Use of anti-(tumour necrosis factor-α) antibody or 3-deaza-adenosine as additives to promote protection by University of Wisconsin solution in ischaemia/reperfusion injury
Chi-Huei CHIANG, Chin-Pyng WU, Wann-Cherng PERNG, Horng-Chin YAN, Cheng-Ping YU; Use of anti-(tumour necrosis factor-α) antibody or 3-deaza-adenosine as additives to promote protection by University of Wisconsin solution in ischaemia/reperfusion injury. Clin Sci (Lond) 1 September 2000; 99 (3): 215–222. doi: https://doi.org/10.1042/cs0990215
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