| In clinical, obstructive jaundice is a common pathologic status, many systemic organs injuries and corresponding pathophysiological changes are induced by obstructive jaundice, which the most important injury is liver damage, and liver damages is also an important inducible factor of other complication. The liver damages induced by obstructive jaundice are multi-aspect, with the deep research on the rules of apoptosis, now researches have demonstrated that cholestasis, active oxygen-derived free radicals, some cytokines, mitochondrial dysfunction are the factors that cause apoptosis of hepatocytes. Researches have revealed that NO involved in the biological adjustments of apoptosis, and plays a double control role in apoptosis. In some cells, NO induce apoptosis; while in some other cells, NO inhibit apoptosis. Until now, there are no reports about the roles of NO on the apoptosis of hepatocytes induced by obstructive jaundice. In this experiment, we have measured the NO content in serum and liver tissues and apoptosis of hepatocytes in rodent obstructive jaundice models, investigated the affect of NO content in serum and liver tissue on the apoptosis of hepatocytes in rodent obstructive jaundice models, and made some more deep discusses on the mechanism of hepatocytes apoptosis induced by NO in the rodent obstructive jaundice models. Material and methods: 54 Wistar rats (male, weight 250g-300g) were divided randomly into (1) Control group (group K): 6 rats were untreated, and allowed free access to water and food. (2) Sham operation group (group S): 18 rats underwent division of common bile duct without ligation, the other treatment were same to obstructive jaundice group. (4) Obstructive jaundice group (group O): 18 rats were anesthetized by 10% chloral hydrate, then the common bile ducts were double ligatized; after operation, the animal were allowed free access to water and food. (4) Obstructive jaundice + L-Arg group (group A): 6 rats were injected with L-Arg (100mg/kg, per day) into abdominal cavity for 7 days on the basis of rodent obstructive jaundice models; (5) Obstructive jaundice + L-NAME group (group N): 6 rats were injected with L-NAME (50mg/kg, per day) into abdominal cavity for 7 days on the basis of rodent obstructive jaundice models; Sham group (group S) and obstructive jaundice group (group O) were then divided into S3, S5, S7, O3, O5 and O7 subgroup according to the days after operation, and every subgroup was assigned 6 rats. The index that be observed included: 1. The general state of health: include mental statue, color pattern, food taking and what have been seen after incision into abdominal cavity. 2. Blood was drawn from inferior vena, the alanine aminotransferase (ALT), aspartate aminatransferase (AST) and total bilirubin (TBil) in serum were measured by automatic biochemistry analyzer. 3 The NO content in serum and liver tissues were measured by nitrate reductase method. 4 The pathological changes in liver tissues were observed by light microscope after HE dyeing. 5. The expression of iNOS mRNA in liver tissue of group K, S and O were determined by hybridization in situ. 6. The apoptosis of hepatocytes were measured by TUNEL. 7. The expression of Fas, Bcl-2, caspase-3 and NF-κBP65 were determined by immune histochemistry. Results: 1.The rats in control group and sham group were agility, and sensitized to pain, there were no changes in the color of skin and urine; after incision into abdominal cavity, we have observed that there were no ascite, the color of liver were bright red, the surface were luster, and the texture of liver were soft. Light microscope revealed that there were no swelled hepatocytes, no cellular necrosis, the liver cell cord were lined up in order. The rats in obstructive jaundice group, group A and N move sluggishly, were insensitive to pain, the color of skin and urine turned into yellow; There were different levels cholestasis in liver, the surface of liver were mattness, there were 0.3cm—0.6cm dilatation in the diameter of commo...
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