Background/aims: During cold preservation of liver grafts, expression of tissue adhesion molecules has been reported as a factor indicative of preservation injury. Some biochemical agents as well as increased levels of intracellular calcium also play important roles in preservation injury during cold storage. In the current study, we aimed to test if the addition of a calcium channel blocker, sodium nitroprusside, or glutathione into preservation solution would reduce upregulation of adhesion molecules, thus leading to decreased preservation injury in the rat liver. Methods: Fifty Albino Wistar rats, weighing 200 50 g, were divided into 1 control (perfused with Wisconsin solution, without preservation) and 4 study groups of rat livers (10 livers each). Livers in study groups were harvested, perfused, and preserved for 16 hours in 4 different solutions (Wisconsin solution alone, Wisconsin solution+verapamil, Wisconsin solution+sodium nitroprusside and Wisconsin solution+glutathione). At the end of the preservation time, levels of graft tissue adhesion molecule (ICAM-1) expression were analyzed. Results: Preservation for 16 hours with Wisconsin solution alone and Wisconsin solution+verapamil perfusates caused significantly more ICAM-1 expression than did preservation for 16 hours with Wisconsin solution+sodium nitroprusside and Wisconsin solution+glutathione perfusates (p=0.010). No significant difference was found in ICAM-1 expression between the Wisconsin solution+sodium nitroprusside and Wisconsin solution+glutathione groups. In the control group, perfusion with Wisconsin solution alone, without preservation, represented minimal ICAM-1 expression, reflecting minimum preservation injury (p=0.0003). Conclusions: Addition of sodium nitroprusside and glutathione into the Wisconsin solution decreased levels of ICAM-1 molecule expression, which reflects lower levels of preservation injury. In this study, the addition of verapamil to the perfusate/preservation solution for reducing the intracellular calcium accumulation had no effect on tissue ICAM-1 molecule expression.