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系统性高血压不能预防啮齿动物模型中慢性眼压升高。

Systemic hypertension is not protective against chronic intraocular pressure elevation in a rodent model.

机构信息

Department of Optometry and Vision Sciences, the University of Melbourne, Parkville, 3010, Victoria, Australia.

出版信息

Sci Rep. 2018 May 8;8(1):7107. doi: 10.1038/s41598-018-25264-4.

Abstract

High intraocular pressure is the most well documented glaucoma risk factor; however many patients develop and/or show progression of glaucoma in its absence. It is now thought that in some instances, ocular perfusion pressure (blood pressure - intraocular pressure) may be as important as intraocular pressure alone. Thus, systemic hypertension would be protective against glaucoma. Epidemiological studies, however, are inconclusive. One theory of why hypertension may not protect against elevated intraocular pressure in spite of increasing ocular perfusion pressure is that with time, morphological changes to the vasculature and autoregulatory failure outweigh the benefits of improved perfusion pressure, ultimately leading to poor retinal and optic nerve head blood supply. In this study we showed the presence of increased wall:lumen ratio and wall area of the ophthalmic artery in rats with chronic hypertension in addition to failure of retinal autoregulation in response to acute modification of ocular perfusion pressure. Subsequently we found that in spite of dramatically increasing ocular perfusion pressure, chronic systemic hypertension failed to protect retinal structure and function from a rodent model of glaucoma.

摘要

高眼压是最有文献记录的青光眼危险因素;然而,许多患者在没有眼压升高的情况下也会发生和/或进展为青光眼。现在认为,在某些情况下,眼球灌注压(血压-眼压)可能与眼压本身同样重要。因此,系统性高血压可能对青光眼有保护作用。然而,流行病学研究尚无定论。尽管眼压升高,但高血压可能无法保护眼睛不受影响的一种理论是,随着时间的推移,血管的形态变化和自动调节失败超过了改善灌注压的益处,最终导致视网膜和视神经头部的血液供应不良。在这项研究中,我们显示了慢性高血压大鼠的眼动脉壁:腔比和壁面积增加,以及对急性眼灌注压变化的视网膜自动调节失败。随后,我们发现尽管眼球灌注压显著升高,但慢性全身性高血压未能保护视网膜结构和功能免受青光眼啮齿动物模型的影响。

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