Reduced retinal vessel response to flicker stimulation but not to exogenous nitric oxide in type 1 diabetes.
OBJECTIVE
Various studies have shown that retinal vessels in patients with diabetes mellitus have a reduced capacity to adapt to changes in perfusion pressure and to stimulation with flickering light. Structural and functional changes in retinal vessels in diabetes could lead to a general reduction of vasodilator and/or vasoconstrictor capacity. To gain more insight into this topic, we compared the response of retinal vessel diameters to systemic glyceryl trinitrate (GTN) and stimulation with diffuse luminance flicker in patients with diabetes and healthy control subjects.


METHODS
Twenty patients with type 1 diabetes mellitus featuring no or mild nonproliferative diabetic retinopathy and 20 healthy, age-matched subjects were included in this study. A vessel analyzer was used for measurement of diameters of retinal arteries and veins. The response of diameters was measured continuously during stimulation with flickering light, as well as immediately after sublingual application of 0.8 mg GTN.


RESULTS
The response of retinal vessels to flickering light was significantly reduced in the patients with diabetes (arteries: 2.9% in diabetes versus 7.0% in control subjects, P < 0.002; veins: 4.6% in diabetes versus 6.8% in control subjects, P = 0.020). GTN-induced vasodilatation was not different between the patients with diabetes and the healthy control subjects (P >or= 0.70).


CONCLUSIONS
The present study confirmed reduced response of retinal vessels to stimulation with flickering light in diabetes. The response of retinal vessels to a direct NO-donor, however, was maintained. This result indicates that abnormal flicker-induced vasodilatation in diabetes is not a consequence of generally reduced retinal vascular reactivity (ClinicalTrials.gov number, NCT00432029).
Departments of Clinical Pharmacology and.
Berthold
B
Pemp
Gerhard
G
Garhofer
Günther
G
Weigert
Katharina
K
Karl
Hemma
H
Resch
Michael
M
Wolzt
Leopold
L
Schmetterer
D000328:Adult; D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure / Q000502:physiology; D003922:Diabetes Mellitus, Type 1 / Q000503:physiopathology*; D003930:Diabetic Retinopathy / Q000503:physiopathology*; D005260:Female; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D007429:Intraocular Pressure / Q000502:physiology; D008297:Male; D009569:Nitric Oxide / Q000494:pharmacology; D005996:Nitroglycerin / Q000494:pharmacology*; D010775:Photic Stimulation; D012171:Retinal Vessels / Q000503:physiopathology*; D014664:Vasodilation / Q000187:drug effects* / Q000528:radiation effects*; D014665:Vasodilator Agents / Q000494:pharmacology; D014792:Visual Acuity
D001786:Blood Glucose; D006442:Glycated Hemoglobin; D009569:Nitric Oxide; D005996:Nitroglycerin; D014665:Vasodilator Agents; C517652:hemoglobin A1c protein, human