Valberg S J, Carlson G P, Cardinet G H, Birks E K, Jones J H, Chomyn A, DiMauro S
Department of Anatomy, School of Veterinary Medicine, University of California, Davis.
Muscle Nerve. 1994 Mar;17(3):305-12. doi: 10.1002/mus.880170308.
Although exertional myopathies are commonly recognized in horses, specific etiologies have not been identified. This is the first report in the horse of a deficiency of Complex I respiratory chain enzyme associated with profound exercise intolerance. Physical examination, routine blood tests, endoscopy, and ultrasonograms of the heart and iliac arteries were unremarkable. With slow, incremental exercise (speeds 1.5-7 m/s), the Arabian mare showed a marked lactic acidosis, increased mixed venous PVO2, and little change in oxygen consumption. Muscle biopsies contained large accumulations of mitochondria with bizarre cristae formations. Biochemical analyses revealed a very low activity of the first enzyme complex in the mitochondrial respiratory chain (NADH CoQ reductase). The exercise intolerance and muscle stiffness in this horse were attributed to a profound lactic acidosis resulting from impaired oxidative energy metabolism during exercise.
虽然运动性肌病在马匹中较为常见，但具体病因尚未明确。本文首次报道了一匹马因复合体I呼吸链酶缺乏而导致严重运动不耐受的病例。体格检查、常规血液检查、内窥镜检查以及心脏和髂动脉的超声检查均未发现异常。在缓慢递增运动（速度1.5 - 7米/秒）过程中，这匹阿拉伯母马出现明显的乳酸酸中毒，混合静脉血氧分压升高，而氧耗量变化不大。肌肉活检显示线粒体大量堆积，嵴形态怪异。生化分析表明线粒体呼吸链中第一种酶复合体（NADH辅酶Q还原酶）的活性极低。这匹马的运动不耐受和肌肉僵硬归因于运动期间氧化能量代谢受损导致的严重乳酸酸中毒。
