Foitzik Thomas, Eibl Guido, Schneider Paul, Wenger Frank A, Jacobi Christoph A, Buhr Heinz J
Department of Surgery, Benjamin Franklin Medical Center, Freie Universität Berlin, Germany.
JPEN J Parenter Enteral Nutr. 2002 Nov-Dec;26(6):351-6. doi: 10.1177/0148607102026006351.
The cytokines involved in the systemic inflammatory response in acute pancreatitis (AP) comprise lipid mediators (eg, prostanoids, thromboxanes, leukotrienes) generated from arachidonic acid (AA) and eicosapentaenoic acid (EPA). The AA-derived mediators are generated from omega-6-fatty acid (FA) and have strong proinflammatory effects and the EPA-derived mediators generated from omega-3-fatty acid are less active or even exhibit anti-inflammatory effects. Basic parenteral nutrition delivers omega-6-FA and omega-3-FA at a ratio of approximately 7:1.
To investigate whether altering the FA composition by fish oil supplementation (omega-3-FA) affects cytokine production and the parameters reflecting systemic disease severity in experimental AP.
Severe AP was induced in 30 rats by standardized intraductal infusion of bile salt and IV cerulein. Six hours after AP induction, rats were randomized to TPN using commercial solutions with identical amounts of glucose, amino acids, and fat but different FA compositions: group 1 received a soybean-based fat solution without additional fish oil and group 2 was supplemented with 0.2 g/kg per day fish oil. TPN was continued for 2 days. Serum concentrations of IL-6 and IL-10 were measured before and after AP induction and at 24 and 48 hours after starting TPN. Routine cardiorespiratory and renal parameters were monitored to assess the systemic response at the organ level.
Animals treated with fish oil had significantly higher IL-10 values (at 24 hours, 63 +/- 7 versus 46 +/- 3 pg/mL), produced more urine (28 +/- 0.9 versus 21 +/- 1.6 mL), and had significantly fewer episodes of respiratory dysfunction (defined as a pO2 < 80 mm Hg or pCO2 > 50 mm Hg for >15 minutes; 29% versus 67%) during the observation period.
Altering eicosanoid mediator precursor availability by infusion of (omega-3 fatty acid increases anti-inflammatory cytokines in this model of AP. This together with improved renal and respiratory function suggests that the systemic response to pancreatic injury is attenuated.
急性胰腺炎（AP）全身炎症反应中涉及的细胞因子包括由花生四烯酸（AA）和二十碳五烯酸（EPA）产生的脂质介质（如前列腺素、血栓素、白三烯）。源自AA的介质由ω-6脂肪酸（FA）产生，具有很强的促炎作用，而源自EPA的介质由ω-3脂肪酸产生，活性较低甚至具有抗炎作用。基础肠外营养提供的ω-6-FA和ω-3-FA比例约为7:1。
研究通过补充鱼油（ω-3-FA）改变脂肪酸组成是否会影响实验性AP中细胞因子的产生以及反映全身疾病严重程度的参数。
通过标准化的胆管内输注胆盐和静脉注射雨蛙肽在30只大鼠中诱导重症AP。AP诱导6小时后，将大鼠随机分为两组接受全胃肠外营养（TPN），使用葡萄糖、氨基酸和脂肪含量相同但脂肪酸组成不同的商业溶液：第1组接受不含额外鱼油的大豆基脂肪溶液，第2组每天补充0.2 g/kg鱼油。TPN持续2天。在AP诱导前后以及开始TPN后24小时和48小时测量血清白细胞介素-6（IL-6）和白细胞介素-10（IL-10）浓度。监测常规心肺和肾脏参数以评估器官水平的全身反应。
接受鱼油治疗的动物IL-10值显著更高（24小时时，63±7 vs 46±3 pg/mL），尿量更多（28±0.9 vs 21±1.6 mL），并且在观察期内呼吸功能障碍发作显著更少（定义为动脉血氧分压<80 mmHg或动脉血二氧化碳分压>50 mmHg持续超过15分钟；29% vs 67%）。
在该AP模型中，通过输注ω-3脂肪酸改变类花生酸介质前体的可用性可增加抗炎细胞因子。这与改善的肾脏和呼吸功能一起表明对胰腺损伤的全身反应减弱。
