Effects of an essential fatty acid defficiency diet on the progrction of acute renal failu

必需脂肪酸缺乏症（EFAD）可改善双侧输尿管梗阻（BUO）发作后24小时出现的GFR和肾血浆流量下降。本实验观察了必需脂肪酸缺乏对大鼠肾组织中PGE_2、6-ketoPGF_1 α和TxB_2的生成以及PGE_2异构酶、PGI_2合成酶、TXB_2和TXB_2的影响，结果表明，必需脂肪酸缺乏对PGE_2、6-ketoPGF_1 α和TXB_2的生成以及PGE_2异构酶、PGI_2合成酶、TXB_2和TXB_2的生成有明显影响。从喂食EFAD饲料或标准饲料约4周的假手术对照（SOC）和BUO大鼠分离的肾小球中的Tx合酶和环氧化酶（考克斯）。BUO大鼠肾小球PGE_2、6-keto-PGF_1 α和TxB_2的生成明显高于SOC大鼠。类二十烷酸的生成速率与PGE_2异构酶、PGI_2合成酶、Tx合成酶和考克斯酶的活性密切相关。另一方面，必需脂肪酸缺乏可抑制BUO大鼠肾小球类二十烷酸生成的增加。给予EFAD饮食的SOC和BUO大鼠类二十烷酸的合成水平相当，表明EFAD使肾小球类二十烷酸的生成正常化。此外，PGE_2异构酶、PGI_2合成酶、Tx合成酶和考克斯的活性在SOC和BUO大鼠之间无显著性差异。因此，我们的研究结果表明，EFAD防止肾小球产生的类花生酸的增加，由于考克斯和类花生酸形成酶在BUO的设置24小时的持续时间的失活。EFAD对BUO大鼠肾功能的保护作用可能部分归因于肾小球类花生酸（尤其是TxA_2）的正常化。

Essential fatty acid defficiency (EFAD) ameliorates the decrease in GFR and renal plasma flow that occurs 24 hours after the onset of bilateral ureteral obstruction (BUO). The vasoactive hormones, prostaglandins (PGs) and thromboxane (Tx), have a role in the changes in renal function described above.Thus, we evaluated the effect of essential fatty acid defficiency on the prodnction of PGE_2,6-keto PGF_1 alpha and TxB_2 and the activities of PGE_2 isomerase, PGI_2 synthase, Tx synthase and cyslooxygenase (COX) in glomeruli isolated from sham-operated control (SOC) and BUO rats fed an EFAD diet or a standard diet for approximately 4 weeks. A standarded diet significantly increased the glomerular production of PGE_2,6-keto PGF_1 alpha and TxB_2 in BUO vs SOC rats. The production rates of eicosanoids correlated well with the activities of PGE_2 isomerase, PGI_2 synthase, Tx synthase and COX.On the other hand, an essential fathy acid defficiency aboloshed the increase in glomerular eicosanoid production seen in rats with BUO.The synthetic levels of eicosanoids were comparable in SOC and BUO rats fed an EFAD diet, indicating normalization of glomerular eicosanoid production duo to EFAD.Moreover, there were no significant differences in the activities of PGE_2 isomerase, PGI_2 synthase, Tx synthase and COX between the SOC and BUO rats. Thus, our results indicate that EFAD prevents the increase in production of eicosanoids by glomeruli due to inactivation of COX and eicosanoid-forming synthases in the setting of BUO of 24 hours duration. The protective effect of EFAD on renal function in rats with BUO may be due in part to normalization of the glomerular production of eicosanoids, particularly TxA_2.