O'Brien P J
Human Safety Department 500 Miami Valley Laboratories, Procter & Gamble, Cincinnati, OH 45253-8707, USA.
Am J Vet Res. 1997 Jan;58(1):11-6.
To test the hypothesis that the derangement of myocardial energy homeostasis characteristic of idiopathic dilated cardiomyopathy (IDCM) of Doberman Pinschers was attributable to deficiency of creatine kinase (CK) isoenzyme MB relative to CK isoenzyme MM and troponin-T (Tn-T).
9 Doberman Pinschers with advanced congestive heart failure attributable to IDCM and 9 mixed-breed dogs without cardiac disease (controls).
Myocardial myofibrillar CK-MM, mitochondrial CK, and cytosolic CK-MB activities were determined in comparison with the concentration of cardiac-specific, myofibrillar protein Tn-T. Myocardial biopsy specimens were obtained after euthanasia and were ultrafrozen. Isoenzymes of CK were separated electrophoretically, and their activity was determined, using a coupled-enzyme, kinetic, fluorescent assay and densitometry. Troponin-T content was determined by immunoassay.
Myofibrillar CK-MM and mitochondrial CK activities and Tn-T content were 25% lower in the dogs with IDCM than in controls, whereas cytosolic CK-MB activity was 50% lower.
Deficiency of CK-MB activity is a component of and may have a central role in the energy deficiency characteristic of failing myocardium in IDCM of Doberman Pinschers. A side-product of this study was the observation that, in dogs, CK-MB activity and Tn-T content of myocardium are sufficiently high to be candidate serum markers for active cardiac injury.
检验以下假设，即杜宾犬特发性扩张型心肌病（IDCM）所具有的心肌能量稳态紊乱是由于肌酸激酶（CK）同工酶MB相对于CK同工酶MM和肌钙蛋白T（Tn-T）缺乏所致。
9只因IDCM导致严重充血性心力衰竭的杜宾犬以及9只无心脏疾病的杂种犬（对照组）。
测定心肌肌原纤维CK-MM、线粒体CK和胞质CK-MB的活性，并与心肌特异性肌原纤维蛋白Tn-T的浓度进行比较。安乐死后获取心肌活检标本并超低温冷冻。采用耦合酶动力学荧光测定法和光密度测定法，通过电泳分离CK同工酶并测定其活性。采用免疫测定法测定肌钙蛋白T含量。
IDCM犬的肌原纤维CK-MM和线粒体CK活性以及Tn-T含量比对照组低25%，而胞质CK-MB活性低50%。
CK-MB活性缺乏是杜宾犬IDCM衰竭心肌能量缺乏的一个组成部分，并且可能在其中起核心作用。本研究的一个附带发现是观察到，在犬类中，心肌的CK-MB活性和Tn-T含量足够高，足以成为活动性心脏损伤的候选血清标志物。
