Kim D N, Schmee J, Baker J E, Lunden G M, Sheehan C E, Lee C S, Eastman A, Solis O, Ross J S, Thomas W A
Department of Pathology and Laboratory Medicine, Albany Medical College, New York 12208.
Exp Mol Pathol. 1993 Oct;59(2):122-35. doi: 10.1006/exmp.1993.1033.
We have investigated in swine the effect of fish oil additives to a butter-cholesterol hyperlipidemic diet (BT) on atherogenesis and thrombogenesis when average plasma cholesterol levels were kept similar in fish oil-treated and untreated BT groups. The studies included evaluation of lesion sizes and cell numbers, counts of adherent monocytes over lesions, and counts of platelet clumps (microthrombi) over lesions either attached directly to endothelium or to adherent monocytes. Anatomic sites studied for lesion development were the left anterior descending coronary artery (LAD), the distal 1/5 of the abdominal aorta, and a proximal portion of the thoracic aorta. Counts of attached monocytes and platelet clumps were made by scanning electron microscopy only for the LAD and expressed per mm2 of surface. The most striking new result was in regard to the platelet clumps. These were reduced by the fish oil from 996 +/- 295/mm2 in the untreated BT group to 313 +/- 59 and 364 +/- 105 in BT+cod liver oil and BT+menhaden oil groups, respectively. Most of the platelet clumps were adherent to attached monocytes in all groups and the number of attached monocytes were greatly reduced by the fish oil additive. Thus there were close relationships among platelet clumps, monocytes, and lesion endothelium. Numbers of attachments over nonlesion endothelium were much less than those over lesions in all dietary groups. The most surprising result was the lack of retardation of lesion growth by the fish oil additives in spite of the reduction in attached monocytes and platelet clumps. In previous studies where the high plasma cholesterol levels in the BT swine had been modestly reduced (about 25%) there had been a marked retardation of lesion growth. The current result suggests that plasma cholesterol is the major factor controlling lesion growth in this model through under milder conditions and longer observation periods other factors might become apparent.
我们在猪身上研究了在鱼油处理组和未处理的黄油 - 胆固醇高脂血症饮食（BT）组平均血浆胆固醇水平保持相似的情况下，向BT饮食中添加鱼油对动脉粥样硬化形成和血栓形成的影响。研究包括评估病变大小和细胞数量、病变上黏附单核细胞的计数以及病变上直接附着于内皮或黏附单核细胞的血小板团块（微血栓）的计数。研究病变发展的解剖部位是左冠状动脉前降支（LAD）、腹主动脉远端1/5以及胸主动脉近端部分。仅对LAD通过扫描电子显微镜进行黏附单核细胞和血小板团块的计数，并以每平方毫米表面面积表示。最显著的新结果是关于血小板团块。在未处理的BT组中，血小板团块数量为996±295/mm²，而在BT + 鳕鱼肝油组和BT + 鲱鱼油组中分别降至313±59和364±105。在所有组中，大多数血小板团块都黏附于黏附的单核细胞，并且鱼油添加剂使黏附单核细胞的数量大幅减少。因此，血小板团块、单核细胞和病变内皮之间存在密切关系。在所有饮食组中，非病变内皮上的附着数量远少于病变上的附着数量。最令人惊讶的结果是，尽管黏附单核细胞和血小板团块减少，但鱼油添加剂并未延缓病变生长。在先前的研究中，BT猪的高血浆胆固醇水平适度降低（约25%）时，病变生长明显延缓。目前的结果表明，在该模型中，血浆胆固醇是控制病变生长的主要因素，不过在更温和的条件下和更长的观察期内，其他因素可能会显现出来。
