青光眼
发病机制
医学
灌注
眼压
眼科
血流
高眼压
心脏病学
内科学
标识
DOI:10.1111/j.1755-3768.2011.3223.x
摘要
Abstract Today, several lines of evidence indicate that beside the classical risk factors such as increased intraocular pressure or family history, decreased ocular perfusion may contribute to the pathogenesis of the disease. In particular, a decrease in ocular blood flow may lead to ischemic events, which in turn may trigger ganglion cell loss and subsequent detoriation of visual field. Recent studies have indicated that instabilities of perfusion rather than a continuous decline of ocular perfusion may be an important factor in the pathogenesis of the disease. In healthy subjects, changes in ocular perfusion pressure are compensated for by an autoregulatory response of the ocular vasculature, in order to keep blood flow constant. This mechanism may be impaired in patients with glaucoma. Indeed several studies indicate that glaucoma patients show reduced vascular reactivity as induced for example by changes in ocular perfusion pressure or by increased metabolic demands. This talk aims to summarize different techniques to test vascular reactivity in humans and the data currently available for patients with glaucoma. In addition, possible pathomechanisms of impaired vascular reactivity will be discussed.
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