AIM: To study the role of nitric oxide and endothelin in myocardial ischemia-reperfusion injury (MIRI) and effect of ligustrazini (LGT). METHODS: The rabbits were randomly divided into three groups (n=10, in each ),sham operated group( A ),MIR group( B ) and LGT group(C).Plasma nitric oxide products( NOP,in terms of NO - 2/NO - 3 ) contents,endothelin (ET) levels,and lactate dehydrogenase (LDH) activities were measured before ischemia, 40 minutes after ischemia and 20 minutes after reperfusion.Meanwhile NOP, ET concentrations and LDH activity in myocardium were measured ,and the ultrastructure changes in myocardium were observed under electron microscope at 20 minutes after reperfusion. RESULTS: As compared with group A,NOP decreased and ET as well as LDH increased at 40 minutes (P

AIM: To study the protective effect of Ligustrazini(LGT) on gut barrier function after hemorrhagic shock-reperfusion. METHODS: Thirty white rabbits were divided randomly into 3 groups: control group (A),shock group (B) and LGT group (C). Malondialdehyde(MDA), tumor necrosis factor-?(TNF ?), interleukin-1?(IL-1?) and nitric oxide products(NO - 2/NO - 3) contents were measured in intestinal mucosa at 3 hours following reperfusion,culture of bacteria in blood from rabbits of 3 groups was carried out,the intestinal mucosa was examined under optical and electron microscope. RESULTS: MDA, TNF ?, IL-1? and NO - 2/NO - 3 contents of intestinal mucosa remained unchanged in group C,but increased significantly in group B, compared with group A. Incidence of bacterial translocation in group B was markedly higher than that in group A at 30 min following reperfusion,there was not any difference between group A and group C. Under light and electronic microscope,in comparison with A and C groups,intestinal mucosa damage in B group became more severe. CONCLUSION: LGT can protect gut barrier from intestinal ischemia-reperfusion injury induced by hemorrhagic shock through reducing oxygen free radicals,raising nitric oxide and preventing inflammation.