Abstract
that had significantly poorer oxygenation during the reperfusion period compared to the other groups (p 0.001). Also, only in the HV group, there were higher tissue interleukin-8 levels (p 0.05) and wet-to-dry ratio (p 0.05) along with histological findings of graft tissue injury than in the control group. There was no significant difference in these parameters between the control, HT and NC groups. Conclusions: Only premortem hypoxia provoked by hypoventilation significantly impaired lung graft function in DCD lung transplantation and the severity exceeded acirculatory warm ischemic injury. Ventilatory rather than circulatory deterioration in the withdrawal phase can trigger the onset of severe warm ischemic injury.
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