RESUMO
An association between hypercholesterolemia and high-frequency hearing loss has been suggested previously. Most data have been epidemiologic, and only recently have experimental studies appeared supporting this observed association. It is unclear whether this hearing loss is related solely to hypercholesterolemia or if it is a consequence of cholesterol-induced vascular changes. The New Zealand White rabbit was used to study the auditory effects of noise, hypercholesterolemia, and the combination of both. Auditory function was evaluated with far-field monitoring of click-evoked auditory brain stem responses by comparing latency/intensity functions and absolute click-evoked thresholds. Hypercholesterolemia was maintained for only 3 weeks, theoretically eliminating atherosclerotic vascular changes as a mechanism contributing to observed changes. Auditory function was unchanged after 3 weeks of hypercholesterolemia. Also, the changes observed after noise exposure were comparable between the normal and the hypercholesterolemic groups. We conclude that if hypercholesterolemia contributes to high-frequency hearing loss, the pathophysiology is related to cholesterol-induced vascular changes, not solely to hypercholesterolemia.
Assuntos
Perda Auditiva de Alta Frequência/etiologia , Perda Auditiva Provocada por Ruído/etiologia , Perda Auditiva/etiologia , Hipercolesterolemia/complicações , Animais , Audiometria de Resposta Evocada , Tronco Encefálico/fisiopatologia , Perda Auditiva de Alta Frequência/fisiopatologia , Perda Auditiva Provocada por Ruído/fisiopatologia , Masculino , CoelhosRESUMO
In the past 5 years much has been learned about the syndrome of ciliary dyskinesia, commonly referred to as immotile cilia syndrome. This syndrome appears to be a congenital defect in the ultrastructure of the cilia, which results in one of three basic defects; lack of dynein arms, absence of radial spokes, or transposition of microtubules. Three cases are presented with electron micrographs; they illustrate the diverse clinical presentations of this disease entity as well as some of the structural abnormalities. The normal and abnormal anatomy of the cilia is discussed and some explanation is offered as to why these structural abnormalities present with such a variety of clinical expressions.
