Oudot F, Grynberg A, Sergiel J P
Unité de Nutrition Lipidique, Institut National de la Recherche Agronomique, Dijon, France.
Am J Physiol. 1995 Jan;268(1 Pt 2):H308-15. doi: 10.1152/ajpheart.1995.268.1.H308.
The synthesis of eicosanoids was investigated in cultured rat ventricular myocytes. Under normoxia, the cardiomyocytes released 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) and prostaglandin (PG) E2 and smaller amounts of PGF2 alpha and thromboxane B2. Hypoxia enhanced the production of PGE2 and PGF2 alpha, whereas the synthesis of 6-keto-PGF1 alpha was not affected. Conversely, posthypoxic reoxygenation greatly increased the synthesis of 6-keto-PGF1 alpha, whereas the synthesis of PGF2 alpha, was not affected and that of PGE2 was reduced. The cardiomyocyte polyunsaturated fatty acid (PUFA) profile was altered by arachidonic acid or eicosapentaenoic acid and docosahexaenoic acid. Under normoxia, the eicosanoid production appeared to be roughly related to the cell phospholipid arachidonic acid content. Conversely, during posthypoxic reoxygenation, the production of eicosanoids was related to the cell phospholipid n-3 PUFA content, with the n-3-rich cells displaying a marked inhibition of the synthesis. This inhibition was mainly attributed to eicosapentaenoic acid and/or docosapentaenoic acid. Whether this inhibition occurs in vivo during postischemic reperfusion, it may contribute to the beneficial effect of n-3 PUFA on the heart.
在培养的大鼠心室肌细胞中研究了类二十烷酸的合成。在常氧条件下，心肌细胞释放6-酮前列腺素F1α（6-酮-PGF1α）和前列腺素（PG）E2，以及少量的PGF2α和血栓素B2。缺氧增强了PGE2和PGF2α的生成，而6-酮-PGF1α的合成未受影响。相反，缺氧后复氧极大地增加了6-酮-PGF1α的合成，而PGF2α的合成未受影响，PGE2的合成则减少。心肌细胞多不饱和脂肪酸（PUFA）谱因花生四烯酸或二十碳五烯酸和二十二碳六烯酸而改变。在常氧条件下，类二十烷酸的生成似乎与细胞磷脂花生四烯酸含量大致相关。相反，在缺氧后复氧期间，类二十烷酸的生成与细胞磷脂n-3 PUFA含量相关，富含n-3的细胞显示出合成的显著抑制。这种抑制主要归因于二十碳五烯酸和/或二十二碳五烯酸。这种抑制在缺血后再灌注期间是否在体内发生，可能有助于n-3 PUFA对心脏的有益作用。
