BACKGROUND & AIMS: Liver resection includes temporal vascular inflow occlusion 
resulting in ischemia/reperfusion injury in the remnant liver. Here, we 
developed a rat model of selective lobe occlusion to isolate reperfusion stress 
from ischemia and to analyze its effect on liver regeneration.
METHODS: Left lateral and median lobes of liver were either mobilized or 
subjected twice for 10min to ischemia followed by 5min reperfusion prior to 
resection while the regenerative lobes were only subjected to reperfusion.
RESULTS: Although intermittent reperfusion stress induced higher levels of serum 
transaminases, analysis of cell cycle regulators revealed accelerated 
regenerative response compared to standard partial hepatectomy. The G0/G1 
transition occurred before tissue resection, as evidenced by c-fos, junB, and 
IL-6 induction. Following hepatectomy, Cyclin D1 up-regulation, G1/S transition, 
and cell division occurred earlier than normal. Unexpectedly, liver 
mobilization, a component of the clamping procedure, also resulted in earlier 
G1/S transition. The shortened G1-phase was driven by the c-Jun N-terminal 
Kinase pathway and was associated with an oxidative stress response as evidenced 
by the expression of inducible nitric oxide synthase.
CONCLUSION: Intermittent selective clamping of lobes to be resected induced 
reperfusion stress on remnant liver that was beneficial for liver regeneration, 
suggesting this procedure could be applied in clinical practice.