The eye and the heart

Abstract

The vasculature of the eye and the heart share several common characteristics. The easily accessible vessels of the eye are therefore—to some extent—a window to the heart. There is interplay between cardiovascular functions and risk factors and the occurrence and progression of many eye diseases. In particular, arteriovenous nipping, narrowing of retinal arteries, and the dilatation of retinal veins are important signs of increased cardiovascular risk. The pressure in the dilated veins is often markedly increased due to a dysregulation of venous outflow from the eye. Besides such morphological criteria, functional alterations might be even more relevant and may play an important role in future diagnostics. Via neurovascular coupling, flickering light dilates capillaries and small arterioles, thus inducing endothelium-dependent, flow-mediated dilation of larger retinal vessels. Risk factors for arteriosclerosis, such as dyslipidaemia, diabetes, or systemic hypertension, are also risk factors for eye diseases such as retinal arterial or retinal vein occlusions, cataracts, age-related macular degeneration, and increases in intraocular pressure (IOP). Functional alterations of blood flow are particularly relevant to the eye. The primary vascular dysregulation syndrome (PVD), which often includes systemic hypotension, is associated with disturbed autoregulation of ocular blood flow (OBF). Fluctuation of IOP on a high level or blood pressure on a low level leads to instable OBF and oxygen supply and therefore to oxidative stress, which is particularly involved in the pathogenesis of glaucomatous neuropathy. Vascular dysregulation also leads to a barrier dysfunction and thereby to small retinal haemorrhages.

<b>Different effect of serotonin on intracellular calcium ion dynamics in the smooth muscle cells between rat posterior ciliary artery and vorticose </b><b>vein </b>

“…10c). The effect of PKI (14)(15)(16)(17)(18)(19)(20)(21)(22) (2 μM) was the same as that observed in the presence of H-89 (n = 8) (data not shown). SQ22536 (100 μM) also completely blocked this increase (n = 8) (Fig.…”

“…Sympathetic nerves from the superior cervical ganglion project to the choroid and, when stimulated, elicit marked vasoconstriction throughout the choroid (39,67). The retinal vasculature shares many anatomical and physiological features with the cerebral and coronary vasculature, which are exposed to similar intrinsic and environmental influences (17,53). Retinal vessel caliber sizes convey different information about systemic diseases, with arteriolar narrowing being associated with elevated blood pressure (10,40,81).…”

“…With the exception of the 5-HT 3 receptor, which is a ligand-gated ion chan-intact arteries and veins were selected and examined under the microscope. Specimens were continuously perfused with HR containing the following agonists and/or antagonists: 5-HT (Nacalai Tesque, 10 μM); GdCl 3 (a nonspecific cation channel blocker; Wako, Japan, 100 μM); diltiazem (a L-type Ca 2+ channel blocker, 40 μM); thapsigargin (a sarco-endoplasmic reticulum Ca 2+ -ATPase inhibitor, 2 μM); U73122 (a phospholipase C inhibitor, 5 μM); SQ22536 (an adenylyl cyclase inhibitor, 100 μM); ketanserin (a 5-HT 2 antagonist, 1 μM); 8-Hydroxy-DPAT (a 5-HT 1a agonist, 50 μM), all from Sigma; CP93129 (a 5-HT 1b agonist, 10 μM); ML 9 (a selective myosin light chain kinase inhibitor, 10 μM); PKI (14)(15)(16)(17)(18)(19)(20)(21)(22) (a cell-permiable protein kinase A (PKA) inhibitor, 2 μM), all from TOCRIS (Minneapolis, MN, USA), α-methylserotonin maleate (a 5-HT 2 agonist, 100 μM); 2-methylserotonin maleate (a 5-HT 3 agonist, 100 μM); and H-89 (a PKA antagonist, 20 μM), all from Enzo Life Sciences (Farmingdale, NY, USA).…”

Endothelial dysfunction in cardiovascular disease and Flammer syndrome—similarities and differences

“…The eye as a direct window to vascular function has an appeal beyond structural assessment [54]. Static and dynamic retinal vessel analyses (RVA) are unique and elegant in several ways.…”

The effect of hemodialysis on intraocular pressure

“…1,2 Altered ocular blood flow was reported to accelerate the development and progression of the disease in such patients; as such, not only elevated IOP, but also medical conditions that negatively affect ocular blood flow will obviously cause ischemia and reperfusion damage in glaucoma patients and in individuals prone to glaucoma. [3][4][5] Hemodialysis (HD) is an important component of the treatment of end-stage renal disease (ESRD). Some studies have reported the effects of HD on IOP, but the findings are inconsistent.…”