Lamers J M, Hartog J M, Verdouw P D, Hülsmann W C
Department of Biochemistry, Medical Faculty, Erasmus University Rotterdam, The Netherlands.
Basic Res Cardiol. 1987;82 Suppl 1:209-21. doi: 10.1007/978-3-662-08390-1_25.
It is widely recognized that dietary polyunsaturated fatty acids (PUFA's) and cholesterol can profoundly influence the development of atherosclerotic plaques in coronary vessels, which may lead to myocardial infarction. The possibility that dietary fatty acids may also directly influence cardiac function has received less attention. We therefore reviewed the evidence of the effects of dietary fatty acids, in particular n-3 and n-6 PUFA's, on myocardial phospholipid fatty acid composition and cardiovascular performance. Heart organelles appear to incorporate uncommon fatty acids like 22:1 and trans- 18:1. Diets enriched with 22:1 induce myocardial lipidosis. N-9, n-6 and n-3 families compete among membrane C20 and C22 acids. Several studies have dealt with the relation between diet-induced changes of cardiac membrane (sarcolemma, sarcoplasmic reticulum and mitochondria) phospholipids and membrane function. In view of the variety of diets used and of the membrane functions studied, the results do not permit equivocal interpretation. Several investigators have reported an altered stress response of the heart due to a change of PUFA's in the diet. In rats fed with a low 18:2n-6/18:3n-3 ratio combined with relatively low amounts of saturated fatty acids, a high incidence of myocardial lesions has been observed. Pigs are less sensitive but more susceptible to the development of vitamin E deficiency, when the dietary PUFA content is high. Increased contractility and coronary flow rate have been reported for Langendorff-perfused hearts of rats fed 18:2n-6-rich diets. The effects on coronary flow rate are possibly related to alterations in eicosanoid synthesis, which may also contribute to the reduction by n-6 or n-3 PUFA's in infarct size, magnitude of recovery of function and suppression of reperfusion arrhythmias following release of a coronary artery ligation. On the other hand, increased peroxidation of membrane lipids, due to their high content of n-3 PUFA, may be deleterious.
人们普遍认识到，膳食中的多不饱和脂肪酸（PUFA）和胆固醇会深刻影响冠状动脉粥样硬化斑块的形成，这可能导致心肌梗死。膳食脂肪酸也可能直接影响心脏功能，这一可能性受到的关注较少。因此，我们回顾了膳食脂肪酸，特别是n-3和n-6多不饱和脂肪酸，对心肌磷脂脂肪酸组成和心血管功能影响的证据。心脏细胞器似乎会纳入不常见的脂肪酸，如22:1和反式-18:1。富含22:1的饮食会诱发心肌脂肪变性。N-9、n-6和n-3家族在膜C20和C22酸之间相互竞争。几项研究探讨了饮食引起的心脏膜（肌膜、肌浆网和线粒体）磷脂变化与膜功能之间的关系。鉴于所使用饮食的多样性和所研究的膜功能，这些结果无法进行明确的解释。几位研究人员报告称，由于饮食中PUFA的变化，心脏的应激反应发生了改变。在喂食低18:2n-6/18:3n-3比例并结合相对少量饱和脂肪酸的大鼠中，观察到心肌病变的高发生率。当膳食PUFA含量高时，猪对维生素E缺乏的发展不太敏感，但更易受影响。据报道，喂食富含18:2n-6饮食的大鼠的Langendorff灌注心脏的收缩力和冠状动脉流速增加。对冠状动脉流速的影响可能与类花生酸合成的改变有关，这也可能有助于减少n-6或n-3多不饱和脂肪酸在冠状动脉结扎解除后的梗死面积、功能恢复程度和再灌注心律失常的抑制。另一方面，由于其高含量的n-3多不饱和脂肪酸导致的膜脂质过氧化增加可能是有害的。
