An experimental study of hepatic ischemia-reperfusion injury

Objective To explore the relationship between liver damage and endogenous nitric oxide (NO) change in experimental hepatic ischemia-reperfusion injury. Methods Eighteen dogs were divided e- qually into two groups namely donor and receptor. Specimen collected before reperfusion, 0.5, 2, 6, and 12 hours after reperfusion. The level of NO in the liver was measured by Griess method. The amount of free calcium ion [Ca~(2+)]i in the liver cells were observed by confocal laser scanning microscopy. The apoptosis of liver cell was assessed by flow cytometry. Results NO was increased at 0.5 h after reperfusion and reached to high level after 6h, and decreased at 12 h (P≤0.01). Water content of liver was also increased continu- ously from 0.5 h, to 6 hours and lasted 12 hours after reperfusion(P≤0.01). [(Ca~(2+)]i was obviously in creased after ischemia-reperfusion (P≤0.01). Animals from I/R groups showed significant increasing in serum ALT at each time of reperfusion. The liver cell apoptosis was obviously increased at 0.5 h, and to a high level at 6 h (P≤O.01). Conclusion Endogenous NO might be participated in the liver damage after ischemia-reperfusion injury in dogs.