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P. Jeppesen, J. Sanye–Hajari, J. Mehlsen, T. Bek; Interaction Between Pressure Autoregulation and Metabolic Autoregulation in Type 2 Diabetic Patients With Minimal Retinopathy . Invest. Ophthalmol. Vis. Sci. 2006;47(13):482.
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© ARVO (1962-2015); The Authors (2016-present)
Changes in retinal perfusion due to disturbances in tone regulation of retinal arterioles are assumed to be involved in the pathogenesis of diabetic retinopathy. It has been shown previously that both pressure autoregulation and metabolic autoregulation may be involved in the disease pathogenesis, but the interaction between these two autoregulatory mechanisms in diabetic retinopathy is unknown.
Twenty type 2 diabetic patients with minimal diabetic retinopathy and 20 pair–wise matched normal persons were studied. The diameter response of retinal vessels was studied using the Retinal Vessel Analyzer (RVA) after the blood pressure had been increased by isometric exercise (pressure autoregulation), after exposure of the retina to 8 Hz flicker stimulation (metabolic autoregulation), and after exposure to these two experimental conditions simultaneously.
An increase in the blood pressure by isometric exercise induced a contraction of the retinal arterioles of –0.8±0.5 % in normal persons, and a dilation of the arterioles 1.0±0.5 % in type 2 diabetic patients. These responses differed significantly (p=0.02). Flicker stimulation induced a significant dilation of the arterioles in normal persons 3.9±0.7% (p<0.001) and a borderline significant dilation in diabetic patients of 1.4 ±0.7 % (p=0.05). Increased blood pressure induced simultaneously with flicker stimulation did not change the diameter response in normal persons. However, in diabetic patients an increase in blood pressure induced by isometric exercise "normalized" the flicker induced vasodilation.
Both pressure autoregulation and metabolic autoregulation of retinal blood flow are disturbed in diabetic retinopathy. However, depending on the experimental conditions these disturbances in autoregulation may both accentuate and counteract each other. This may potentially help understanding the background for disturbances in retinal perfusion in diabetic retinopathy.
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