CAJ | 학술논문

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12 h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12 h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.
목적 탐토감유삼지대대서중증이선염ET-1、NO표체급병리평분적영향.방법 건강SD대서36지,수궤분위2조,매조18지.A조:고지혈증조;B조:비고지혈증조.고지혈증통과고지사료위양3주형성,중증급성이선염통과5%적우황담산납역행이담관주사제작.A、B량조대서분별우중증급성이선염성모전、후4、8화12 h취혈측정감유삼지、정분매、ET-1화NO농도,병취이선조직경HE염색병이학검사,진행이선병이학평분.결과 B조성모후감유삼지명현증고(P＜0.05),A、B량조성모후각시점ET-1급NO농도균명현증고(P＜0.05),A조ET-1재4、8량시점증고경명현(P＜0.05).ET-1、NO재12 h시점A、B량조균정하강추세,이A조하강경명현.A조각시점이선병이학평분균명현고우B조(P＜0.05).결론 고감유삼지조건하중증이선염ET-1화NO승고경조、경가명현,고감유삼지가가중중증급성이선염이선적병리손해.
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.