Objective SD rat models of stomach-heat syndrome were established to further investigate the physiopathological mechanism of stomach-heat syndrome.Methods Under certain laboratory condition,criteria of stomach-heat syndrome for the animal models were set up firstly.Then decoction of Rhizoma Zingiberis was given to the rats for modeling.Two weeks after modeling,the symptoms of the rats were observed and pathological and biochemical examination was carried out.Weireqing capsules were used to confirm the success of the establishment of stomach-heat syndrome in rats.Results Two weeks after modeling,the model rats had the symptoms of thirst with preference for drinking and reddened tongue.Congestion in gastric mucosa occurred and the levels of 6-keto-PGF1?and TXB2 in the model group were higher than those in the control group.However,in model rats pretreated with Weireqing,the symptoms and signs of stomach-heat syndrome and histological changes were relieved.Conclusion Under the controlled laboratory condition,feeding rats with decoction of Radix Zingiberis can be successfully used to establish animal model of human stomach-heat syndrome .

Objective To investigate the histological and ultrastructural characteristics of liver graft after different warm ischemia time (WIT) in rats. Methods According to WIT, rats were randomized into 7 groups, with WIT of 0, 10, 15, 20, 30, 45, 60 minutes respectively. All specimens were investigated by light, electron microscopy, and histochemistry stain. 6, 24, and 48 hours after orthotopic liver transplantation(OLTx) ,the graft morphology was observed. Results The donor liver from non-heart-beating donors (NHBO) underwent ischemia injury both in the warm ischemia period and in the reperfusion period. Morphological changes were positively related to warm ischemia time in a time-dependent manner during the reperfusion period. There was a histocytic degeneration of different degree within 30 minutes warm ischemia. Although becoming more severe with the prolongation of warm ischemia time within this period, there was no obvious hepatocyte necrosis in any specimens. In WIT 45 min group, small focal necrosis occurred which was found in central area of hepatic lobule first. In 60 min group, patchy or diffused necrosis was observed and the area was gradually extended, while hepatic sinusoid endothelial cell obviously swelled to be bleb or balloonlike, hepatic sinusoid was obstructed and microcirculation was in disorder. Conclusion Rat liver graft undergoing warm ischemia injury is on the reversible stage within 30 minutes warm ischemia time by histological, histochemistry and ultrastructural dynamic observation. 45 min is a critical point of rat liver graft to endure warm ischemia injury, and when WIT was over 60 min, the damage is irreversible.