April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
Flicker-induced retinal vasodilatation is not dependent on complement factor H polymorphism in healthy young subjects
Author Affiliations & Notes
  • Gerhard Garhofer
    Department of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria
  • Reinhard Told
    Department of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria
    Center for Medical Physics and Biomedical Engineering, Medical University of Vienna, Vienna, Austria
  • Stefan Palkovits
    Department of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria
  • Agnes Bolz
    Department of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria
    Center for Medical Physics and Biomedical Engineering, Medical University of Vienna, Vienna, Austria
  • Helmuth Haslacher
    Department of Laboratory Medicine, Medical University of Vienna, Vienna, Austria
  • Leopold Schmetterer
    Department of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria
    Center for Medical Physics and Biomedical Engineering, Medical University of Vienna, Vienna, Austria
  • Footnotes
    Commercial Relationships Gerhard Garhofer, None; Reinhard Told, None; Stefan Palkovits, None; Agnes Bolz, None; Helmuth Haslacher, None; Leopold Schmetterer, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 4344. doi:
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      Gerhard Garhofer, Reinhard Told, Stefan Palkovits, Agnes Bolz, Helmuth Haslacher, Leopold Schmetterer; Flicker-induced retinal vasodilatation is not dependent on complement factor H polymorphism in healthy young subjects. Invest. Ophthalmol. Vis. Sci. 2014;55(13):4344.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: We have previously shown that in healthy homozygous carriers of the complement factor H (CFH, rs1061170) tyrosine 402 histidine (Y402H) variant, which is known to be a risk factor for age related macula degeneration (AMD), choroidal blood flow regulation is altered. No evidence is currently available on whether the complement factor H polymorphism may also affect blood flow regulation of the retinal circulation. This study was performed to investigate whether flicker induced vasodilation is altered in subjects carrying complement factor H polymorphism.

Methods: A total of 100 healthy subjects (aged between 18 and 45 years) were included in this study. Retinal blood flow regulation was tested by assessing retinal vessel calibers in response to stimulation with flicker light. Flicker responses were determined with a dynamic vessel analyzer (DVA). In addition, genotyping for rs1061170 was performed.

Results: Out of the 99 subjects included in the study, 18 were homozygous for the risk allele C, 50 were homozygous for the ancestral allele T and 31 subjects were heterozygous (CT). One subject had to be excluded from the study, since no genetic analysis could be performed due to technical difficulties. Baseline diameters of retinal arteries (p=0.62) and veins (p=0.47) were comparable between the three groups. Flicker induced vasodilation in both retinal arteries (p=0.38) and retinal veins (p=0.62) was comparable between the three studied groups.

Conclusions: Our data indicate that homozygous healthy young carriers of the C risk allele at rs1061170 do not show abnormal flicker-induced vasodilation in the retina. This indicates, that, in contrast to the choroidal circulation, where an abnormal blood flow regulation in the choroid was seen, the retinal circulations does not show an impaired response to visual stimulation. Whether this is due to the differences of the vasculature bed, differences of innervation or the fact that different stimuli were used remains unclear.

Keywords: 436 blood supply • 688 retina • 691 retina: proximal (bipolar, amacrine, and ganglion cells)  
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