Saladino C F, Klein R A, Jonas E A
Department of Medicine, Nassau County Medical Center, East Meadow, New York 11554.
Artery. 1987;14(5):304-15.
It has been demonstrated by us and other workers that rats receiving I.V. infusions of Lipofundin-S will develop aortic changes indicative of early atherosclerosis. However, different lipid emulsions which are used in the clinical setting for parenteral nutrition vary substantially in chylomicron size and fatty acid composition. Therefore, in an attempt to better understand the mechanism by which a lipid emulsion might induce vessel lesions, we compared the nature of potential aortic changes resulting from infusions of Liposyn, Intralipid, or Lipofundin-S into the tail veins of Sprague-Dawley rats. Three groups of animals received either Liposyn (N = 10), Intralipid (N = 5), or Lipofundin-S (N = 9) at the rate of 6 g fat/kg body wt/day for 10 consecutive days. A fourth group (N = 5) received saline in equivalent dose to evaluate the effect of injection volume on vessel lesion formation. The other controls (N = 6) received no injections. Rats were sacrificed 24 hrs after the last infusion, and 1 mm rings from the top of the aortic arch and proximal third of the thoracic aorta were prepared for transmission electron microscopy (TEM). Examination by TEM allows two main conclusions to be drawn for both segments of the aorta. First, all three emulsions are capable of inducing early vessel changes which include endothelial damage, platelet adherence to damaged endothelium or subendothelial collagen, intimal phagocytic cells, and intimal smooth muscle cells surrounded by collagen bundles and elastin plates. Saline-infused rats only show occasional subendothelial swelling. None of the above-described changes are seen in any of the uninjected controls. Second, Lipofundin-S induces smooth muscle penetration of the intima in 7 of 9 rats, while Liposyn causes such changes in 2 of 10 animals. This difference in the efficiency with which the two emulsions induce the most advanced changes is statistically significantly by Chi Square (p less than 0.05). Intralipid produces smooth muscle penetration of the intima in 2 of 5 rats. The composition of the three emulsions suggests that the lower percent of linoleic acid and larger chylomicron size in Lipofundin-S may account for these differences, at least in part.
我们及其他研究人员已证实，接受静脉输注力保肪宁-S的大鼠会出现表明早期动脉粥样硬化的主动脉变化。然而，临床用于肠外营养的不同脂质乳剂在乳糜微粒大小和脂肪酸组成上有很大差异。因此，为了更好地理解脂质乳剂可能诱发血管病变的机制，我们比较了向斯普拉格-道利大鼠尾静脉输注力补金、英脱利匹特或力保肪宁-S后潜在主动脉变化的性质。三组动物连续10天以6克脂肪/千克体重/天的速率分别接受力补金（N = 10）、英脱利匹特（N = 5）或力保肪宁-S（N = 9）。第四组（N = 5）接受等量生理盐水以评估注射体积对血管病变形成的影响。其他对照组（N = 6）不进行注射。在最后一次输注后24小时处死大鼠，并制备主动脉弓顶部和胸主动脉近端三分之一处的1毫米血管环用于透射电子显微镜（TEM）检查。通过TEM检查可得出关于主动脉这两个节段的两个主要结论。首先，所有三种乳剂都能够诱发早期血管变化，包括内皮损伤、血小板黏附于受损内皮或内皮下胶原、内膜吞噬细胞以及被胶原束和弹性蛋白板包围的内膜平滑肌细胞。输注生理盐水的大鼠仅偶尔出现内皮下肿胀。在任何未注射的对照组中均未观察到上述变化。其次，力保肪宁-S在9只大鼠中有7只诱发内膜平滑肌穿透，而力补金在10只动物中有2只出现此类变化。两种乳剂诱发最严重变化的效率差异经卡方检验具有统计学意义（p小于0.05）。英脱利匹特在5只大鼠中有2只出现内膜平滑肌穿透。三种乳剂的成分表明，力保肪宁-S中亚油酸百分比更低且乳糜微粒更大，这可能至少部分解释了这些差异。
