Recipient treatment with L-arginine attenuates donor lung injury associated with hemorrhagic shock

Organ donors are frequently trauma victims, but the impact of donor hemorrhagic shock and resuscitation (HSR) on pulmonary graft function has not been assessed. L-arginine treatment during reperfusion increases the production of endothelial nitric oxide and thus ameliorates ischemia-reperfusion injury. Objective of the present porcine study was to investigate the effect of donor hemorrhage on pulmonary graft function and potential beneficial effects of L-arginine administration.

In the control-group (n=6), lungs were harvested from donors without hypotensive periods. In the HSR-group (n=6) and HSR-Arg-group (n=6), donors were subjected to hemorrhagic shock (40% blood shed) and resuscitation before harvest. Left lungs were transplanted after hypothermic preservation of 18 hr, and graft function was observed for 6 hr after reperfusion. Recipients in the HSR-Arg-group received a bolus of L-arginine (50 mg/kg BW) intravenously 5 min before reperfusion followed by a continuous intravenous administration of L-arginine 200 mg/kg BW for 2 hr. Tissue specimens and bronchoalveolar lavage fluid were obtained at the end of the observation period.

Donor lung function did not differ between study groups. Compared with the control group, pulmonary graft gas exchange was significantly impaired in the HSR-group. Graft function in the HSR-Arg-group did not differ from control organs. Neutrophil fraction, protein content, and malondialdehyde levels in the bronchoalveolar lavage fluid in the HSR-group were higher compared with control and HSR-Arg-Group.

Although fulfilling ideal donor criteria, pulmonary graft function of lungs harvested from donors subjected to HSR is impaired, but improves significantly when l-arginine is administered during reperfusion.