Lax D, Zhang S L, Li Y, Williams L, Staley N A, Noren G R, Einzig S
Department of Pediatrics, University of Minnesota, Minneapolis 55455.
Cardiovasc Res. 1990 Jul;24(7):540-6. doi: 10.1093/cvr/24.7.540.
The aim of the study was to determine if reduced heart lipid peroxidation in 1-2 month old turkeys with furazolidone induced dilated cardiomyopathy is drug related and model dependent, a non-specific characteristic of the dilated turkey heart, or if alterations of heart lipid peroxidation can occur prior to onset of cardiac dilatation, and therefore may be involved in its pathogenesis.
Ventricular lipid peroxidation capacity and superoxide dismutase activity were measured in controls and in turkeys with spontaneous cardiomyopathy at various ages (newly hatched, 7-10 d, and 1-2 months) and stages of the disease.
46 turkeys with naturally occurring dilated cardiomyopathy and 29 age matched controls were used at hatch, 7-10 d, and 1-2 months of age.
Heart lipid peroxidation, measured by thiobarbituric acid reactive substances (malondialdehyde), was found to be reduced not only in the dilated hearts of 1-2 months old cardiomyopathic turkeys [114(SEM 10) v 176(21) nmol.100 mg-1 protein, p = 0.023] but also in the non-dilated hearts of 9-10 day old cardiomyopathic turkeys [135(17) v 274(35) nmol.100 mg-1 protein, p = 0.004]. Ventricular superoxide dismutase activity was similar in control and cardiomyopathic turkeys at all stages and there was the expected increase with age. In control turkeys ventricular superoxide dismutase activity in 1-2 month old birds, at 718(52) nitrite units.100 mg-1 protein, was significantly higher than values in 7-10 day old turkeys [398(31) nitrite units.100 mg-1 protein, p = 0.001].
Decreased lipid peroxidation capacity is present in the dilated hearts of spontaneously cardiomyopathic turkeys. However, it is also decreased in cardiomyopathic turkeys at 9-10 d (the time of highest mortality) prior to the onset of cardiac dilatation. Therefore, alterations in heart lipid composition may be involved in the pathogenesis of this cardiomyopathy and not simply a result of the cardiac dilatation/hypertrophy process.
本研究旨在确定,在患有由呋喃唑酮诱发的扩张型心肌病的1至2月龄火鸡中,心脏脂质过氧化作用降低是与药物相关且依赖于模型,是扩张型火鸡心脏的非特异性特征,还是心脏脂质过氧化作用的改变会在心脏扩张发作之前发生,因此可能参与其发病机制。
在不同年龄(刚孵化、7至10日龄、1至2月龄)和疾病阶段的对照组以及患有自发性心肌病的火鸡中,测量心室脂质过氧化能力和超氧化物歧化酶活性。
46只患有自然发生的扩张型心肌病的火鸡和29只年龄匹配的对照组火鸡在孵化时、7至10日龄以及1至2月龄时被使用。
通过硫代巴比妥酸反应性物质(丙二醛)测量发现,不仅在1至2月龄患有心肌病的火鸡的扩张心脏中脂质过氧化作用降低[114(标准误10)对176(21)nmol·100mg⁻¹蛋白质,p = 0.023],而且在9至10日龄患有心肌病的火鸡的未扩张心脏中也降低[135(17)对274(35)nmol·100mg⁻¹蛋白质,p = 0.004]。在所有阶段,对照组和患有心肌病的火鸡的心室超氧化物歧化酶活性相似,并且随着年龄增长有预期的增加。在对照组火鸡中,1至2月龄鸟类的心室超氧化物歧化酶活性为718(52)亚硝酸盐单位·100mg⁻¹蛋白质,显著高于7至10日龄火鸡的值[为398(31)亚硝酸盐单位·100mg⁻¹蛋白质,p = 0.001]。
在患有自发性心肌病的火鸡的扩张心脏中存在脂质过氧化能力降低的情况。然而,在9至10日龄(死亡率最高的时期)患有心肌病的火鸡在心脏扩张发作之前脂质过氧化作用也降低。因此,心脏脂质组成的改变可能参与了这种心肌病的发病机制,而不仅仅是心脏扩张/肥大过程的结果。