Abeywardena M Y, Charnock J S
CSIRO, Division of Human Nutrition, Glenthorne Laboratory, O'Halloran Hill, Australia.
Lipids. 1995 Dec;30(12):1151-6. doi: 10.1007/BF02536617.
Several different edible oils were compared for their ability to modify eicosanoid biosynthesis following experimentally-induced myocardial ischemia and reperfusion in the rat. Two types of palm oil [neutralized, bleached, and deodorized (NBDPO) and refined, bleached, and deodorized (RBDPO)] and partially hydrogenated soybean oil (SBO) were tested against a diet supplemented with sunflower seed oil (SSO) rich in n-6 polyunsaturated fatty acids (PUFA). Fish oil (FO) rich in n-3 PUFA, with its known cardioprotective actions, served as an internal reference point for the study. Test oils were fed as a 12% (w/w) supplement for nine months before the induction of myocardial ischemia and reperfusion. Palm oil diets exerted effects indistinguishable from the SBO group against cardiac arrhythmia, which occurred following alterations to coronary blood flow. Arrhythmic potentials, as expressed by a hierarchical scale (0-9) of arrhythmia score, were: SSO, 1.5 +/- 0.5; FO, 0.9 +/- 0.4; SBO, 3.1 +/- 0.5*; NBDPO, 3.2 +/- 0.5*; RBDPO, 3.3 +/- 0.6*; P < 0.05 vs. SSO. Following ischemia and reperfusion, both SSO and RBDPO groups tended to show an increase in myocardial prostacyclin, with the effect being more prominent in the RBDPO group (SSO, 10%; RBDPO, 25%). Thromboxane production was reduced in the FO group. Interestingly, cardiac muscle from both FO and palm oil groups displayed a reduced capacity to produce 12-hydroxyeicosatetraenoic acid SSO, 591 +/- 95.8; SBO, 375.5 +/- 48.9; NBDPO, 287.2 +/- 64.7; RBDPO, 230.9 +/- 80.2**; FO, 203.7 +/- 81.4** (ng/g dry wt, *P < 0.05, **P < 0.01). No clear relationship was seen between the availability of 20:4n-6 in myocardial phospholipids and eicosanoid profile. Data suggests that fatty acid composition of edible oils is not the only determinant of arrhythmic vulnerability and eicosanoid production.
比较了几种不同食用油在大鼠实验性诱导心肌缺血和再灌注后改变类花生酸生物合成的能力。将两种类型的棕榈油[中和、漂白和脱臭（NBDPO）以及精炼、漂白和脱臭（RBDPO）]和部分氢化大豆油（SBO）与富含n-6多不饱和脂肪酸（PUFA）的葵花籽油（SSO）补充饮食进行了测试。富含n-3 PUFA且具有已知心脏保护作用的鱼油（FO）作为该研究的内部参考点。在诱导心肌缺血和再灌注前九个月，将测试油作为12%（w/w）的补充剂喂食。棕榈油饮食对冠状动脉血流改变后发生的心律失常产生的影响与SBO组难以区分。心律失常电位以心律失常评分的分级量表（0-9）表示为：SSO，1.5±0.5；FO，0.9±0.4；SBO，3.1±0.5*；NBDPO，3.2±0.5*；RBDPO，3.3±0.6*；与SSO相比，P<0.05。缺血和再灌注后，SSO和RBDPO组心肌前列环素均有升高趋势，RBDPO组更为明显（SSO，10%；RBDPO，25%）。FO组血栓素生成减少。有趣的是，FO组和棕榈油组的心肌产生12-羟基二十碳四烯酸的能力均降低（SSO，591±95.8；SBO，375.5±48.9；NBDPO，287.2±64.7；RBDPO，230.9±80.2**；FO，203.7±81.4**（ng/g干重，*P<0.05，**P<0.01）。心肌磷脂中20:4n-6的可用性与类花生酸谱之间未发现明显关系。数据表明，食用油的脂肪酸组成不是心律失常易感性和类花生酸产生的唯一决定因素。
