甘油三酯对大鼠重症胰腺炎内皮素和一氧化氮表达及病理评分的影响

目的探讨甘油三酯对大鼠重症胰腺炎ET-1,NO表达及病理评分的影响。方法健康SD大鼠36只，随机分为2组，每组18只。A组：高脂血症组；B组：非高脂血症组。高脂血症通过高脂饲料喂养3周形成，重症急性胰腺炎通过5％的牛黄胆酸钠逆行胰胆管注射制作。A、B两组大鼠分别于重症急性胰腺炎成模前、后4、8和12h取血测定甘油三酯、淀粉酶、ET-1和NO浓度，并取胰腺组织经HE染色病理学检查，进行胰腺病理学评分。结果B组成模后甘油三酯明显增高（P〈0．05），A、B两组成模后各时点ET-1及NO浓度均明显增高（P〈0．05），A组ET-1在4、8两时点增高更明显（P〈0．05）。ET-1、NO在12h时点A、B两组均呈下降趋势，以A组下降更明显。A组各时点胰腺病理学评分均明显高于B组（P〈0．05）。结论高甘油三酯条件下重症胰腺炎ET-1和NO升高更早、更加明显，高甘油三酯可加重重症急性胰腺炎胰腺的病理损害。

Effects of hypertriglyceridemia on NO, ET-1 and the grade of the pathology severity in rats with severe acute pancreatitis

Objective To explore influence of hypertriglyceridemia on serum NO ET-1 and the grade of the pathology severity in rats with severe acute pancreatitis. Methods 36 SD rats were randomly divided into 2 groups, group A (HLSAP group) , group B (SAP group). Severe acute pancreatitis was constructed by retrograde injection of 5% na-taurocholate. Blood samples were taken from all subjects to measure triglyceride, ET-1 and NO, pancreatic tissue samples were taken from head of pancreas and stained with H. E. , the degree of pancreatic damage was observed according to the point score of Schmidt and Pozsar's methods. Results In group A, the concentration of ET-1 increased more obviously than that in group B at 4 hour and 8 hour period(P ＜0. 05). The concentration of NO declined both in group A and group B at 12 hours period,but it had a great decline in group A. Animals with hyperlipidemia and severe acute pancreatitis developed significantly higher(P ＜0. 05) ET-1 than the animals of the non-hyperlipamic severe acute pancreatit group in 4 hours and 8 hours period. NO declined in group A and group B at 12 hours period, group A have significantly higher(P ＜0. 05) decline than group B in NO. The histological degree of pancreatic damage were significantly higher in group A than that in the group B at all times. Conclusions Mircrocirculation disorder had existed disorder in the early of SAP. Hypertriglyceridemia could incrase ET-1 and NO earlier and higher in severe acute pancreatitis, and then decline in the late stage. Hypertriglyceridemia intensified the pathologichistological degree of pancreatic damage.