Isensee H, Jacob R
Institute of Physiology II, University of Tübingen, Germany.
J Cardiovasc Risk. 1994 Dec;1(4):353-9.
Independently of the problem of atherogenesis, the amount and type of fat intake influences the risk of cardiac arrhythmias. However, the relative effectiveness of different fats and the underlying mechanisms are controversial. The aim of the present study was to compare the effects of various oil-enriched diets on the risk of ventricular arrhythmias in rat hearts under conditions of ischaemia and reperfusion and to help clarify the mechanisms underlying the differing effects of the oils on the occurrence of arrhythmias.
Over a 10-week period, we studied five groups of young male Wistar rats given a low-fat chow diet or one enriched with 10% hydrogenated coconut oil, corn oil, linseed oil or sardine oil. Electrocardiograms were recorded from the isolated hearts (Langendorff preparation) perfused with a modified Krebs-Henseleit solution. Ischaemia was induced by a 20 min occlusion of the left anterior descending coronary artery. In another series of experiments, a 10 min occlusion was followed by a 20 min reperfusion period. The times between the first occurrence of extrasystole and the incidence of ventricular tachycardia and fibrillation were determined. The size of the ischaemic zone was assessed using malachite green. The fatty acid composition of the myocardial tissue was analysed using gas chromatography.
An increase in the risk of ventricular arrhythmias under conditions of both ischaemia and reperfusion was obvious in the rats that consumed large quantities of saturated fatty acids (coconut oil) and in the group with a very low intake of fat. Polyunsaturated fatty acids (PUFAs), particularly fish oil, exerted a protective effect. The incidence of ventricular fibrillation was 75% in the low-fat group, 67% in the coconut-oil group, 44% in the corn-oil group, 40% in the linseed-oil group and 10% in the fish-oil group. The time until the first occurrence of extrasystole, the incidence of ventricular tachycardia and the incidence of reperfusion-induced ventricular fibrillation were influenced in a similar manner. The size of the ischaemic zone was significantly reduced in the groups given diets enriched with PUFAs. All protective effects were abolished, however, by cyclooxygenase inhibition with aspirin. The fatty acid composition of myocardial tissue, the ratio of n-3 to n-6 fatty acids and the double-bond index were significantly affected by the various diets.
Whereas saturated fatty acids are obviously proarrhythmic, diets enriched with n-6 or n-3 PUFAs both exert antiarrhythmic effects. Although n-3 fatty acids seem to be more effective, cardioprotection cannot simply be related to the replacement of n-6 by n-3 fatty acids in cardiac membrane phospholipids, given the beneficial effects of corn oil. In any case, replacement of n-3 by n-6 fatty acids is not the underlying mechanism. The overall reduction of prostaglandin formation cannot be the primary mechanism because the beneficial effects of diets rich in PUFAs were abolished by cyclooxygenase inhibition. We conlcude that, besides prostacyclin (PGI2 or PGI3), membrane fluidity and accompanying alterations in functional membrane proteins (e.g. protection from calcium overload) are key factors apart from vascular effects that influence the size of the ischaemic zone.
独立于动脉粥样硬化形成问题之外，脂肪摄入量及其类型会影响心律失常风险。然而，不同脂肪的相对有效性及其潜在机制存在争议。本研究旨在比较各种富含油类的饮食对缺血再灌注条件下大鼠心脏室性心律失常风险的影响，并有助于阐明这些油类对心律失常发生产生不同影响的潜在机制。
在10周的时间里，我们研究了五组年轻雄性Wistar大鼠，分别给予低脂普通饲料或富含10%氢化椰子油、玉米油、亚麻籽油或沙丁鱼油的饲料。从用改良的克雷布斯 - 亨塞尔特溶液灌注的离体心脏（Langendorff制备）记录心电图。通过闭塞左前降支冠状动脉20分钟诱导缺血。在另一系列实验中，先闭塞10分钟，然后再灌注20分钟。确定早搏首次出现的时间以及室性心动过速和颤动的发生率。使用孔雀石绿评估缺血区域的大小。使用气相色谱分析心肌组织的脂肪酸组成。
在摄入大量饱和脂肪酸（椰子油）以及脂肪摄入量极低的大鼠组中，缺血和再灌注条件下室性心律失常风险均明显增加。多不饱和脂肪酸（PUFA），特别是鱼油，具有保护作用。低脂组室颤发生率为75%，椰子油组为67%，玉米油组为44%，亚麻籽油组为40%，鱼油组为10%。早搏首次出现的时间、室性心动过速的发生率以及再灌注诱导的室颤发生率受到类似影响。给予富含PUFA饮食的组中缺血区域大小显著减小。然而，用阿司匹林抑制环氧化酶后，所有保护作用均被消除。各种饮食显著影响心肌组织的脂肪酸组成、n - 3与n - 6脂肪酸的比例以及双键指数。
饱和脂肪酸明显促心律失常，而富含n - 6或n - 3多不饱和脂肪酸的饮食均具有抗心律失常作用。尽管n - 3脂肪酸似乎更有效，但鉴于玉米油的有益作用，心脏保护不能简单地与心脏膜磷脂中n - 3脂肪酸取代n - 6脂肪酸相关。无论如何，n - 6脂肪酸取代n - 3脂肪酸不是潜在机制。前列腺素生成的总体减少不可能是主要机制，因为富含PUFA饮食的有益作用在抑制环氧化酶后被消除。我们得出结论，除前列环素（PGI2或PGI3）外，膜流动性以及伴随的功能性膜蛋白改变（例如防止钙超载）是除血管效应外影响缺血区域大小的关键因素。
