Kennedy S, Rice D A
Department of Pathology, Veterinary Research Laboratory, Belfast, Northern Ireland.
Vet Pathol. 1992 Mar;29(2):129-38. doi: 10.1177/030098589202900205.
We developed an experimental model of nutritional degenerative myopathy in ruminant cattle. Fourteen experimental calves were fed a diet low in vitamin E and selenium for 127 to 137 days. Six of these calves were then euthanatized. After 127 days, a dietary additive of linseed oil that had been treated to protect it against ruminal hydrogenation was added to the low vitamin E and selenium diet of the eight remaining calves as a source of polyunsaturated fatty acids. Six of these animals were euthanatized after 6 to 11 days of polyunsaturated fatty acid feeding; the other two died after 6 and 8 days. Macroscopic myocardial alterations were seen in five polyunsaturated fatty acid-fed calves but not in any other experimental calf. Microscopic lesions, comprising multifocal or diffuse cardiocyte degeneration and necrosis, were seen in atrial and ventricular myocardium of all experimental calves. These changes were more severe in polyunsaturated fatty acid-fed calves than in animals that did not receive polyunsaturates. Ultrastructurally, sublethally damaged cardiocytes had lysed contractile material; vacuolated sarcoplasm; altered mitochondria, sarcoplasmic myelin figures, and lipofuscin granules; and multiple nuclei. Necrotic cardiocytes had contracted myofibrils, pyknotic nuclei, mineralized mitochondria, and plasmalemmal disruption; the external lamina remained largely intact. Necrosis was followed by macrophage invasion and phagocytosis of necrotic debris. Repair of the lesions was by deposition of collagen and elastin fibers. No alterations were seen in the hearts of control calves fed vitamin E and selenium-supplemented diet. The induced myocardial lesions are similar to those of spontaneous nutritional degenerative myopathy in ruminant cattle.
我们建立了反刍动物牛营养性退行性肌病的实验模型。14头实验小牛被喂食低维生素E和硒的饲料127至137天。然后对其中6头小牛实施安乐死。127天后，将经过处理以防止瘤胃氢化的亚麻籽油作为多不饱和脂肪酸的来源添加到其余8头小牛的低维生素E和硒饲料中。在喂食多不饱和脂肪酸6至11天后，对其中6头动物实施安乐死；另外两头分别在6天和8天后死亡。在5头喂食多不饱和脂肪酸的小牛中观察到宏观心肌改变，而在其他实验小牛中未观察到。在所有实验小牛的心房和心室心肌中均可见微观病变，包括多灶性或弥漫性心肌细胞变性和坏死。这些变化在喂食多不饱和脂肪酸的小牛中比未接受多不饱和脂肪酸的动物更为严重。超微结构上，亚致死性损伤的心肌细胞有溶解的收缩物质；空泡化的肌浆；改变的线粒体、肌浆髓鞘样结构和脂褐素颗粒；以及多个细胞核。坏死的心肌细胞有收缩的肌原纤维、固缩的细胞核、矿化的线粒体和质膜破裂；外板基本保持完整。坏死之后是巨噬细胞浸润和坏死碎片的吞噬。病变的修复通过胶原蛋白和弹性纤维的沉积进行。在喂食补充维生素E和硒饲料的对照小牛心脏中未观察到改变。诱导的心肌病变与反刍动物牛自发性营养性退行性肌病的病变相似。
