| Objective: Acute pancreatitis is a kind of common surgical acute abdomen, actuely morbility, tendency of disease rapidly, high incidence rate of MODS. Recently we consider SAP oneself as a kind of severe systemic inflammatory response syndrome and gradually realize that mediators of inflammation and cytokine have decisive effectiveness in the evolution and development of pancreatitis. NO that is a kind of free radical cytokine has a considerly effect in the impairment mechanism of SAP. But, because the interaction of cytokine's reaction network is so anfractuous and the mechanism is so various, that the researchs of specific mechanism action havn't conduct deeply and overall. This article factitious induced rat's SAP by animal experiment. Resperectly to pre-surpply with the substrate of NO or the inhibitor of NOS alter the level of NO in rat body. By analyzing the relationship between the change of NO level, the prognosis turnover of SAP and impairment of pancreas and lung in SAP rat, we study the merchanism and effective pathway of NO during the evolution process and development of SAP. That is to provid a new theory base for the clinical therapy and to seek for a new efficient therapeutic method. Method: 48 Sprague-Dawley rat of 13-15 week age male and body weight 350-450g were randomly devided into 4 group, Group A was sham operatio group(n=12). Group B was the severe acute pancreatitis group (n=12). Group C was the Arginine pretreat group (n=12). Group D was the the sulphuric acid aminoguanidine pretreat group (n=12). All animal were anaesthesiaed by intraperitoneal injecting 2.5% ketamine 0.3ml/100g in Preoperative of five minutes. Group A was opened abdomon by operating and induced actue pancreatitis by turbulencing pancreas. Group B, C, D (each group animal number n=12) was established by injecting of 5% sodium taurocholate (0.15ml/100g) under pancreatic capsule. Group C was therapeutic group and intraperitoneal injected with L-Arginine (250mg/Kg) at 30 minutes before induction of pancreatitis. Group D was therapeutic group and intraperitoneal injected with sulphuric acid aminoguanidine (15mg/Kg) at 30 minutes before induction of pancreatitis. All animals were subcutaneously with 0.9% sodium 5ml/h after induction of pancreatitis. Animal were killed at 4h, 8h, 12h and accordingly divided to 3 batch (each batch number of group A, B, C, D n=4). The serum, BALF (bronchoalveolar lavage flu) and pancreas, lung were reserved in -80℃.We observe and research the viaratio of inflammatory mediators (IL-6, NO), MPO activity of pancreas, MPO activity of lung and the serumal concentration of protein, the BALF concentration of protein and the wet weight of lung, the dry weight of lung. The pathology of lung and pancreas were observed. The serum IL-6 concentrationwas detected by ELISA; the serum NO concentration was detected by colorimetry. The serum protein concentration was detected by Coomassie brilliant blue method. The protein BALF concentration was detected by Coomassie brilliant blue method. (Lung permeability index= the protein BALF concentration /the protein serum concentration). The lung dry weight was weighed after toasted 24 hour in 80℃.(The lung weight ratio = the lung wet weight /the lung dry weight). For analysis of test results, we used the SAS system by computer. Results: The serum IL-6 and NO, the concentration of MPO in pancreas and the concentration of MPO in lung, the lung permeability index,the lung weight ratio in each group expressed by x ±s: NO:Group A(SO):12.45±5.55;Group B(SAP):66.30±17.34;Group C(L-arg):25.10±4.22;Group D(AG):36.04±7.9. IL-6:Group A (SO):44.65±5.01;Group B(SAP):240.60±60.65;Group C(L-arg):132.62±24.91;Group D(AG):116.83±21.56;the concentration of MPO in pancreas:Group A (SO):7.46±3.36;Group B(SAP):61.14±18.54;Group C(L-arg):24.86±6.01;Group D(AG):36.04±7.99;the concentration of MPO in lung:Group A (SO):23.00±9.57;Group B(SAP):84.77±8.20;Group C(L-arg):57.41±11.77;Group D(AG):50.55±8.47;the lung permeability index:Group A (SO):9.83±3.30;Group B(SAP):18.36±1... |
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