The effect of nitric oxide production by sinusoidal endothelial cells on preservation injury during cold ischemia.

Multifactorial elements are responsible for preservation and reperfusion injury in liver allografts. Sinusoidal endothelial cells (SECs) are a primary target of cold preservation injury of the liver. We examined the correlation between nitric oxide (NO) production by SECs and their injury during cold preservation. SECs were isolated from rat livers and preserved in either Euro-Collins (EC) or University of Wisconsin (UW) solution. Injury to the SECs was more severe when preserved in the EC solution than in the UW solution during cold ischemia. In addition, NO production by SECs was found to be proportionate to the cell injury. Cell viability was not improved by the addition of NO inhibitor, L-NMMA. Further, NO inhibitor was detrimental to the SECs in a 24-h preservation in UW solution. LDH release by SECs preserved in UW solution supplemented with L-NMMA was 11.10+/-2.03 IU/l, while that in UW solution alone was 3.70+/-0.70 IU/l (P<0.01). Together, our results suggest that NO protects SECs during cold preservation and that NO from SECs may have beneficial effects on the liver during cold ischemia.