This Article  • References  • Full text PDF  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on HighWire  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Social Bookmarking   What's this?

Implications for Ischemic Disorders of the Retina and Optic Nerve Head

Sohan Singh Hayreh, MD, PhD, DSc; Donald J. Piegors; Donald D. Heistad, MD

Arch Ophthalmol. 1997;115(2):220-228.

Abstract
Background
Ischemic disorders of the retina and optic nerve head, which constitute a common cause of visual loss, are usually seen in patients with atherosclerosis.

Objective
To test the hypothesis that serotonin, which is released when platelets aggregate, may produce vasospasm in atherosclerotic monkeys and, thus, may contribute to the ischemic disorders and that short-term dietary treatment of atherosclerosis causes the propensity to vasospasm to subside.

Methods
We studied the response of retinal and posterior ciliary circulation to serotonin in 18 atherosclerotic (25 eyes) and 5 normal (8 eyes) cynomolgus monkeys. The eyes were evaluated by color fundus photography and fluorescein fundus angiography. The eyes were examined under basal conditions and, at a different time, during the intravenous infusion of serotonin. In 6 of the 18 atherosclerotic animals, the evaluation was repeated 5 to 12 months after discontinuing the atherogenic diet (ie, the regression group).

Results
Serotonin had no effect in normal monkeys. In 18 atherosclerotic monkeys, serotonin produced transient occlusion or delayed filling of the central retinal artery and/or posterior ciliary artery (PCA) in 9 eyes of 9 animals, involving the central retinal artery in 5, lateral PCA in 8, and medial PCA in 5, in various combinations. In 6 animals (6 eyes) of the regression group, the vasoconstrictor effect of serotonin was abolished completely, except in the medial PCA in 1 eye.

Conclusions
Serotonin, in the presence of atherosclerotic lesions, can cause transient, complete occlusion or impaired blood flow in the central retinal artery and/or PCA. We speculate that this mechanism may play a role in the development of ischemic disorders of the retina and optic nerve head. Discontinuing the atherogenic diet abolished or markedly improved the serotonin-induced vasoconstriction within a few months.

Author Affiliations
From the Departments of Ophthalmology (Dr Hayreh) and Internal Medicine and Pharmacology (Mr Piegors and Dr Heistad), University of Iowa College of Medicine, Iowa City.

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Blood pressure and glaucoma
Costa et al.
Br J Ophthalmol 2009;93:1276-1282.
ABSTRACT | FULL TEXT  

Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency in Nonarteritic Anterior Ischemic Optic Neuropathy in a Sardinian Population, Italy
Pinna et al.
IOVS 2008;49:1328-1332.
ABSTRACT | FULL TEXT  

Blindness in the Intensive Care Unit: Possible Role for Vasopressors?
Lee et al.
Anesth. Analg. 2005;100:192-195.
ABSTRACT | FULL TEXT  

Influence of Experimental Chronic High-Pressure Glaucoma on Age-Related Macular Degeneration in Rhesus Monkeys
Jonas and Hayreh
IOVS 2000;41:2972-2977.
ABSTRACT | FULL TEXT  

Localised retinal nerve fibre layer defects in chronic experimental high pressure glaucoma in rhesus monkeys
Jonas and Hayreh
Br J Ophthalmol 1999;83:1291-1295.
ABSTRACT | FULL TEXT