Since the first use of nitroglycerin 120 years ago, NO donors are still important therapy for ischemic cardiovascular diseases. However, the mechanisms of action of NO in ischemia reperfusion injury are still unclear. In the present study, we used a model of hepatic ischemia-reperfusion (I/R) to examine the effect of NO on early phase cytokine production. The left and medium lobes of the liver which occupy approx. 75% of liver wt. were subjected to 30 min of ischemia by clamping relevant artery, followed by 4 h reperfusion by removal of the vascular clamp. The animals were divided into three groups: control, ischemia-reperfusion (I/R); and I/R + L-NAME (10 mg/kg, iv, 10 min prior reperfusion). The results indicated that L-NAME significantly decreased plasma NO levels compared to I/R group. However, the ALT activity in the I/R with L-NAME group was significantly increased. The ratios of iNOS, TNF-α and IL-1β to GAPDH mRNA extracted from the ischemic lobes of I/R with L-NAME were significantly increased compared with I/R groups. In Situ-RT-PCR analysis also showed that the TNF-α mRNA was significantly increased in the endothelium and inflammatory cells in the liver of I/R with L-NAME animals. Conclusion: endogenous NO can reduce ischemic-reperfusion tissue injury may be through the effect on the early phase cytokine generation.
|Original language||English (US)|
|State||Published - Mar 20 1998|
All Science Journal Classification (ASJC) codes
- Molecular Biology