Smith P, Hurst G, Heath D, Drewe R
Histopathology. 1986 Aug;10(8):831-40. doi: 10.1111/j.1365-2559.1986.tb02581.x.
A woman of 62 years with Turner's syndrome died in congestive cardiac failure secondary to a large ventricular septal defect with biventricular hypertrophy. During her last few months the lifelong left-to-right shunt underwent reversal exposing her carotid bodies to hypoxaemia. The carotid bodies were not enlarged, thus demonstrating that hyperplasia of glomic tissue is not brought about by increased myocardial mass per se. They were, however, abnormally cellular with more dark cells ( a variant of chief cells), many of which were abnormally large and showed ultrastructural features of metabolic activity. These changes may represent the earliest histological response of the carotid body to hypoxaemia and later, the dark cells may mature into the more familiar and common light variant. It seems likely that this dark cell activity precedes, probably by a long period, the sustentacular cell hyperplasia and proliferation of nerve axons which we have reported elsewhere as the chronic reaction of the carotid bodies to hypoxaemia.
一名62岁的特纳综合征女性死于充血性心力衰竭,病因是巨大室间隔缺损伴双心室肥厚。在她生命的最后几个月里,终生存在的左向右分流发生了逆转,导致她的颈动脉体暴露于低氧血症中。颈动脉体未增大,因此表明球旁组织增生并非由心肌质量本身增加所致。然而,它们的细胞异常,暗细胞(主细胞的一种变体)增多,其中许多暗细胞异常大,并表现出代谢活动的超微结构特征。这些变化可能代表了颈动脉体对低氧血症的最早组织学反应,随后,暗细胞可能会成熟为更常见的亮细胞变体。这种暗细胞活动很可能在很长一段时间之前就已出现,早于我们在其他地方报道的作为颈动脉体对低氧血症慢性反应的支持细胞增生和神经轴突增殖。