OCULAR FLUID COMPOSITION AND OCULAR TISSUE PHYSIOLOGY

这是一个综合计划的延续，旨在阐明 正常眼内液成分的稳态机制， 房水动力学，并确定改变的作用， 眼内微环境-由于病理生理或 的渗透性和运输功能的病理变化， 血眼屏障-在（年龄依赖性）眼部病理学中。 我们将 继续我们以前开始的一些工作（例如 前列腺素和其他运输过程中的眼内稳态），但我们 将重点测试和阐明一系列 在赠款期间提出假设。 这些假设，大多数 这与我们的进化分歧假说直接相关， 眼防御机制，陈述或暗示以下内容：在一些 物种，尤其是兔，血屏障（BAB）的破坏 代表了一种复杂的（autocoid介导的）递送机制， 用于角膜修复的凝血（和可能的其他）因子; 依赖于高视力的物种，BAB分解发生较少 容易，但纤维蛋白原和其他蛋白质可以进入前房 通过角膜穿透后的泪小管返流;有效的BAB 破裂和泪小管返流取决于前葡萄膜和角膜缘周围 充血;刺激诱导充血， 这些位点由类似的机制介导，并且可能由相同的 眼内炎症发作可导致 血液运输特性的长期或永久性变化 眼屏障，并因此在眼内微环境中，从而 导致诸如慢性单纯性青光眼，老花眼， 老年性白内障和黄斑囊样水肿。 更好地了解眼部刺激和炎症反应， 这些反应中的物种差异不仅会让理性的 选择适用于人类眼部疾病的动物模型，但将 促进这些手术和治疗方法的发展， 疾病和这些方法的适应兽医 眼科 更好地理解这种反应的机制 鉴于越来越多的需要， 一种复杂而积极的手段， 在越来越长寿的人群中。

This is a continuation of an integrated program designed to elucidate the mechanisms of the homeostasis of normal intraocular fluid composition and aqueous humor dynamics and to determine the role of alterations in intraocular micro-environments - as a result of pathophysiological or pathological changes in the permeability and transport functions of the blood-ocular barriers - in (age-dependent) ocular pathologies. We will continue some of our work initiated previously (such as the role of Prostaglandin and other transport processes in ocular homeostasis), but we will focus on testing and elucidating the implications of a set of hypotheses developed during that grant period. These hypotheses, most of which directly relate to our hypothesis of evolutionary divergence in ocular defense mechanisms, state or imply the following: that in some species, especially rabbits, breakdown of the blood acueous barrier (BAB) represents a sophisticated (autocoid mediated) mechanism for the delivery of clotting (and possibly other) factors for corneal repair; that in species which depend on high visual acuity, BAB breakdown occurs less readily, but fibrinogen and other proteins can enter the anterior chamber by canalicular reflux after corneal penetration; that effective BAB breakdown and canalicular reflux depend on anterior uveal and perilimbal hyperemia, respectively; that irritation-induced hyperemia at either of these sites is mediated by a similar mechanism, and possibly by the same autacoids; that episode(s) of intraocular inflammation can cause long-lasting or permanent changes in the transport properties of the blood ocular barrier and, hence, in the intraocular microenvironment, thereby contributing to such disorders as chronic simple glaucoma, presbyopia, senile cataracts and cystoid macular edema. A better understanding of ocular irritative and inflammatory responses and of species differences in these responses will not only allow the rational selection of applicable animal models for human ocular disorders, but will facilitate the development of surgical and therapeutic approaches to these disorders and the adaptation of these approaches to veterinary ophthalmology. A better understanding of the mechanisms of such responses and their control is clearly required in view of the need for increasingly sophisticated and aggressive means of extending the period of useful vision in an increasingly longevous population.