MURPHY G E
J Exp Med. 1952 Mar;95(3):319-32. doi: 10.1084/jem.95.3.319.
Almost invariably these experimental lesions and very frequently the myocardial Aschoff bodies studied in their early stages have been shown to originate in and evolve from lesions of heart muscle fibers. The mono-, multi-, and non-nuciested cell masses, most characteristic of myocardial disease of the rheumatic type, appear to be damaged muscle fibers their fragments, and syncytial cell masses of probable muscular origin that proliferate from beneath the sarcolemma and in the tracks of damaged muscle fibers in reaction to that damage. In addition to destructive changes in cardiac muscle fibers an attempt at myofiber regeneration may occur in some myocardial Aschoff bodies. The most distinguishing histologic feature of the myocardial Aschoff bodies in rheumatic heart disease are the peculiar lesions of muscle fibers. Therefore, it is proposed that they be designated as myofiber Aschoff bodies in order to indicate their origin more accurately. The results of these investigations contrast with the widely accepted theory that all myocardial Aschoff bodies originate as injured interstitial collagen, and that, as they evolve, they consist of damaged interstitial collagen intermingled with cells of non-myogenic derivation that proliferated in response to that collagen injury. These studies, furthermore, provide evidence that experimental homologues of rheumatic myocardial Aschoff bodies have been induced in a very few among many rabbits subjected to reposted focal infections with group A streptococci of different serological types. Hence, they support the concept that the myocardial Aschoff bodies of rheumatic fever are induced by repeated infections with group A streptococci of several different serological types; even though only a certain few among the many patients so infected develop these lesions.
对兔实验性诱导的心肌阿绍夫小体样病变以及多位活动性风湿热患者的多个心肌阿绍夫小体进行组织病理学发病机制的比较研究,结果如下:几乎无一例外,这些实验性病变以及在早期阶段研究的心肌阿绍夫小体,常被证明起源于心肌纤维病变并由其演变而来。风湿性心肌病最具特征性的单核、多核和无核细胞团,似乎是受损的肌纤维、其碎片以及可能源于肌肉的合胞体细胞团,这些细胞团从肌膜下增殖,并在受损肌纤维的轨迹中对损伤做出反应。除了心肌纤维的破坏性变化外,一些心肌阿绍夫小体中可能会出现肌纤维再生的尝试。风湿性心脏病中心肌阿绍夫小体最显著的组织学特征是肌纤维的特殊病变。因此,建议将它们命名为肌纤维阿绍夫小体,以便更准确地表明其起源。这些研究结果与广泛接受的理论形成对比,该理论认为所有心肌阿绍夫小体均起源于受损的间质胶原,并且在演变过程中,它们由受损的间质胶原与因胶原损伤而增殖的非肌源性来源的细胞混合组成。此外,这些研究提供了证据,表明在许多接受不同血清型A组链球菌反复局部感染的兔子中,只有极少数诱导出了风湿性心肌阿绍夫小体的实验同源物。因此,它们支持这样一种概念,即风湿热的心肌阿绍夫小体是由几种不同血清型的A组链球菌反复感染诱导产生的;尽管在众多受感染的患者中只有少数人会出现这些病变。