Prevention of cold ischaemia-reperfusion injury by an endothelin receptor antagonist in experimental renal transplantation.

Conclusions. We conclude that cold ischaemia and preservation damage induces an increase in renal ET Background. Endothelin ( ET ) is known to play a role in the pathogenesis of warm ischaemic renal damage, mRNA and irET expression in the reperfusion phase, contributing both to the deterioration of renal function however, little is known about its involvement in renal cold ischaemia. This study was designed to investigate and to tubular necrosis. Bosentan is eVective in protecting kidneys from this cold ischaemia‐reperfusion the response of ET after kidney cold ischaemia, and to assess the potential protective eVect of bosentan, a damage. Non-selective ET A/ ET B receptor antagonists might be potentially useful in clinical renal dual, non-selective ET A /ET B receptor antagonist, against cold ischaemia‐reperfusion injury in a rat transplantation. model of syngeneic renal transplantation.