Cold preservation of liver allografts injures hepatic sinusoidal linin
g cells. This injury is exacerbated on reperfusion, in part because of
adhesion of leukocytes. Platelets also adhere to activated endothelia
l surfaces. In this study we examined the role of platelets in preserv
ation injury. Our specific aim was to determine whether the degree of
platelet adhesion on reperfusion of preserved rat livers was related t
o duration of cold or warm ischemia and whether platelet adhesion resu
lted in injury to allografts. We also examined the effect of prior act
ivation of platelets on adhesion and injury. Rat livers were preserved
at 1-degrees-C for different time periods in University of Wisconsin
solution and then reperfused for 3 hr on the isolated perfused rat liv
er system with Krebs-Henseleit solution to which unactivated isolated
rat platelets were added. Other livers were rewarmed before reperfusio
n or reperfused with activated platelets. Platelets were lost from the
circulation in all studies; the percentage reduction of circulating p
latelets was dependent on the length of preservation. The initial plat
elet concentration did not affect the rate of reduction of platelets i
n the circuit. Rewarming before reperfusion increased platelet adheren
ce, and prior activation also increased adherence. With electron micro
scopy we determined that platelets adhered in small aggregates to endo
thelial cells or endothelial cell remnants. Adherent platelets appeare
d more activated and contained fewer granules than did unperfused plat
elets. Liver injury as measured by release of transaminases into perfu
sate was worsened by longer periods of cold preservation and by additi
on of rewarming to the protocol. The presence of platelets under these
circumstances aggravated injury. Prior activation of platelets also i
ncreased the extent of injury. These studies show that platelets have
an important role in cold preservation-reperfusion injury.