| Objective:Through the establishment of acute on chronic liver failure(ACLF) rats model, gastrointestinal motility, gastrointestinal hormone, gastric antrum, jejunum smooth muscle cell intracellular calciumion concentration ([Ca2+]i) of rats in acute on chronic liver failure, to clarify the changes of gastrointestinal motility may be "the pathological process of liver disease spread to the spleen", through the traditional Chinese medicine Yiqi Jianpi early intervention, effect of Jianpi drugs on the gastrointestinal motility disorder caused by the changes and pathology of acute on chronic liver failure during the study,"may be a possible mechanism of reinforcing the spleen in the treatment of liver disease".Methods:The Wistar rats were randomly divided into4groups:normal group, model group, control group(Jiedu Huayu granule), experimental group (Jiedu Huayu and jianpi granule). Immunological hepatic fibrosis was induced by administration of bovine serum albumin to Wistar rats. D-galactosamine was simultaneously intraperitoneally injected to establish the ACLF models. The experiment group was treated with Jiedu Huayu granule, in bovine serum albumin attack also Jianpi granule to the death of former7days by intragastric administration for the treatment of granule, control group before being killed in7days with the Jiedu Huayu granules intragastrically treated. The rats of normal group were put to death after intraperitoneal injection, and the rest of the group were put them to death after being modeled. Then the Serum transaminase (ALT, AST) level, pathological changes in liver tissues, portal vein endotoxin, motilin, gastric residual rate and intestinal propelsive rate, antrum of stomach, intestinal [Ca2+]i were detected for each group.Result: 1. The normal group were alive, and no death, the model group, control group, experimental group were dead10,8and7respectively, mortality rates were50%,40%,35%, because of the small sample size, no statistical analysis.2. Compared with the normal group, the model group ALT and AST were significantly increased, the difference was statistically significant (P<0.01); compared with the model group, the control group and experimental group ALT, AST were lower, both statistical difference between the groups significance (P<0.01or P<0.05); compared with the control group, the experimental group ALT, AST decreased, the difference was statistically significant (P<0.05).3. Results of liver pathology:The normal group the structure of hepatic lobule is complete, liver cells arranged in neat and orderly, as the center of central vein radially, liver cell degeneration and necrosis, cholestasis and hepatic sinusoidal cells were hyperplasia, no inflammatory cells in portal area and heterogeneous cells. The model group can be seen in hepatic sinusoid congestion, the structure of hepatic lobule was destroyed, liver cell necrosis, bridging necrosis, infiltration of inflammatory cells in portal area, extensive fibrous tissue hyperplasia. The control group and the experimental group compared with the model group, the pathological changes of liver cells reduce, flaky, spotty necrosis, portal area extensive degeneration of liver cells, a small amount of fibrous tissue hyperplasia.4. Results of colon tissue pathology:Compared with the normal group, the levels of endotoxin in portal vein of rats in the model group was significantly increased, the differences was statistically significant (P<0.01); Compared with the model group, endotoxin levels in the control group were decreased, but not statistically significant (.P>0.05), were significantly decreased endotoxin difference in the experimental group, the difference was statistically significant (P<0.01); Compared with the control group, the experimental group endotoxin levels were decreased significantly (PO.01).5. Results of motilin:Compared with normal group, the motilin of rats in model group was higher, the differences was statistically significant (P<0.01); Compared with the model group, the control group MTL levels were increased, but the difference was not statistically significant (P>0.05), MTL levels were elevated in the experimental group, the difference was statistically significant (P<0.01); and the control group compared to the experimental rats MTL levels were elevated, and the difference was statistically significant (P<0.01).6. Results of gastric residual rate and intestinal propulsive rate:Compared with the normal group, the model group rats gastric residual rate increased significantly, small intestinal propulsion rate decreased significantly (P<0.01); Compared with the model group, the control group decreased gastric residual rate, intestinal propulsive rate was increased, but the difference was not statistically significant (P>0.05), the experimental group decreased gastric residual rate, intestinal propulsive rate were increased, the difference was statistically significant (P<0.01); Compared with the control group, the experimental group decreased gastric residual rate, intestinal propulsive rate increased, the difference was statistically significant (P<0.05or P<0.01).7. Results of the [Ca2+]j of smooth muscle of gastric antrum and jejunum: Compared with the normal group, the model group, gastric antrum and jejunum smooth muscle [Ca2+]i decreased, the difference was statistically significant (P<0.01); Compared with the model group, the control group and experimental group of gastric antrum and jejunum smooth muscle [Ca2+]i increased, the difference was statistically significant (P<0.05or P<0.01); Compared with the control group rats in the experimental group, gastric antrum and jejunum smooth muscle [Ca2+]i levels were elevated, the difference was statistically significant ((P<0.05).8. Correlation analysis:the gastric residual rate and MTL, gastric antrum, jejunumsmooth muscle [Ca2+]i was found, and the negative correlation (r=-0.518, P<0.01; r=-0.344, P<0.05; i=-0.391, P<0.01); small intestinal propulsion rate and MTL, gastric antrum, jejunum smooth muscle [Ca2+]i was found, and the positive correlation (r=0.646, P<0.01; r=0.543, P<0.01; r=0.599, P<0.01); gastric residual rate, intestinal propulsive rate and endotoxin were correlated, and negative correlation (r=0.483, P<0.01; r=-0.613,P<0.01). Conclusion:1. Acute on chronic liver failure rat gastric emptying and small intestinal propulsive function weakened, gastrointestinal motility disorder that exists.2. The blood plasma motilin level decreased of Acute on chronic liver failure rats, gastric antrum and jejunum smooth muscle decreased [Ca2+]i, endotoxin increased significantly, suggesting acute on chronic liver failure and the disorder of gastrointestinal hormones in gastric and intestinal smooth muscle cell contractility cause gastrointestinal motility disorder "one of the pathological process and mechanism of liver disease spread to the spleen"3. Early drug intervention treatment with invigorating the spleen, gastrointestinal motiliy can obviously improve the acute on chronic liver failure in rats, so as to reduce intestinal endotoxemia, reduce the pathological damage of liver tissue, liver failure to achieve, is "one of the mechanisms of reinforcing the spleen in the treatment of liver disease". |
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