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抗青光眼药物对高眼压兔眼血流的影响。

Effects of antiglaucoma drugs on ocular blood flow in ocular hypertensive rabbits.

作者信息

Chiou G C, Chen Y J

机构信息

Department of Medical Pharmacology and Toxicology, Texas A&M University College of Medicine, College Station.

出版信息

J Ocul Pharmacol. 1993 Spring;9(1):13-24. doi: 10.1089/jop.1993.9.13.

DOI:10.1089/jop.1993.9.13
PMID:8096537
Abstract

Antiglaucoma drugs were studied systematically on the ocular blood flow in ocular hypertensive rabbits. As expected, pilocarpine, clonidine and acetazolamide were all found to increase the ocular blood flow in the retina and choroid. However, their use in the clinics was much less than the beta-blockers, such as L-timolol, levobunolol, betaxolol and metipranolol. It was surprising to find that all non-specific and beta 1-specific adrenergic blockers decreased the ocular blood flow in ocular hypertensive rabbits. If this finding holds true in human patients, the use of beta-blockers for glaucoma treatment should be reconsidered. Dopamine antagonists, such as droperidol, metoclopramide and loxapine, were found to increase the ocular blood flow. Therefore, they might be able to replace beta-blockers for glaucoma treatment.

摘要

对青光眼药物进行了系统研究,观察其对高眼压兔眼血流的影响。不出所料,毛果芸香碱、可乐定和乙酰唑胺均能增加视网膜和脉络膜的眼血流量。然而,它们在临床上的使用远少于β受体阻滞剂,如左旋噻吗洛尔、左布诺洛尔、倍他洛尔和美替洛尔。令人惊讶的是,所有非特异性和β1特异性肾上腺素能阻滞剂均会降低高眼压兔的眼血流量。如果这一发现适用于人类患者,那么应重新考虑使用β受体阻滞剂治疗青光眼。发现多巴胺拮抗剂,如氟哌利多、甲氧氯普胺和洛沙平,能增加眼血流量。因此,它们或许能够替代β受体阻滞剂用于青光眼治疗。

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Effects of antiglaucoma drugs on ocular blood flow in ocular hypertensive rabbits.抗青光眼药物对高眼压兔眼血流的影响。
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引用本文的文献

1
Effects of antiglaucoma drugs on blood flow of optic nerve heads and related structures.抗青光眼药物对视神经头和相关结构血流的影响。
Jpn J Ophthalmol. 2013 Mar;57(2):133-49. doi: 10.1007/s10384-012-0220-x. Epub 2013 Jan 16.
2
Effects of dopamine on retinal and choroidal blood flow parameters in humans.多巴胺对人体视网膜和脉络膜血流参数的影响。
Br J Ophthalmol. 2007 Sep;91(9):1194-8. doi: 10.1136/bjo.2006.113399. Epub 2007 Mar 23.
3
Acquired color vision loss and a possible mechanism of ganglion cell death in glaucoma.青光眼患者后天性色觉丧失及神经节细胞死亡的一种可能机制。
Trans Am Ophthalmol Soc. 2000;98:331-63.