Hayreh S S, Piegors D J, Heistad D D
Department of Ophthalmology, University of Iowa College of Medicine, Iowa City, USA.
Arch Ophthalmol. 1997 Feb;115(2):220-8. doi: 10.1001/archopht.1997.01100150222012.
Ischemic disorders of the retina and optic nerve head, which constitute a common cause of visual loss, are usually seen in patients with atherosclerosis.
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.
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).
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.
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.
视网膜和视神经乳头的缺血性疾病是视力丧失的常见原因,常见于动脉粥样硬化患者。
检验血小板聚集时释放的血清素可能在动脉粥样硬化猴中引起血管痉挛,进而可能导致缺血性疾病,以及短期饮食治疗动脉粥样硬化可使血管痉挛倾向消退这一假说。
我们研究了18只动脉粥样硬化食蟹猴(25只眼)和5只正常食蟹猴(8只眼)的视网膜及睫状后循环对血清素的反应。通过彩色眼底照相和荧光素眼底血管造影对眼睛进行评估。在基础条件下以及在静脉输注血清素期间的不同时间对眼睛进行检查。在18只动脉粥样硬化动物中的6只,在停止致动脉粥样硬化饮食后5至12个月重复评估(即消退组)。
血清素对正常猴无影响。在18只动脉粥样硬化猴中,血清素在9只动物的9只眼中导致视网膜中央动脉和/或睫状后动脉(PCA)短暂闭塞或延迟充盈,以各种组合形式累及视网膜中央动脉5只眼、外侧PCA8只眼和内侧PCA5只眼。在消退组的6只动物(6只眼)中,血清素的血管收缩作用完全消失,只有1只眼的内侧PCA除外。
在存在动脉粥样硬化病变的情况下,血清素可导致视网膜中央动脉和/或PCA短暂、完全闭塞或血流受损。我们推测这种机制可能在视网膜和视神经乳头缺血性疾病的发生中起作用。停止致动脉粥样硬化饮食在几个月内消除或显著改善了血清素诱导的血管收缩作用。