Toke Bek1, Javad Hajari, Peter Jeppesen. 1. Department of Ophthalmology, Arhus University Hospital, DK-8000 Arhus C, Denmark. toke.bek@mail.tele.dk
Abstract
BACKGROUND: Diabetic retinopathy is accompanied with changes in the autoregulation of retinal blood flow secondary to changes in the systemic blood pressure and the retinal metabolism. In the present study we tested the working hypothesis that there is an interaction between these mechanisms that might be relevant for understanding and treating flow disturbances in diabetic retinopathy. METHODS: Fifty-four persons divided into three age and sex matched groups were studied: Group 1: twenty normal persons. Group 2: fourteen patients with type 2 diabetes mellitus and no diabetic retinopathy. Group 3: twenty type 2 diabetic patients with minimal diabetic retinopathy and a diabetes duration similar to that of the patients in group 2. Using the Retinal Vessel Analyzer (RVA) the diameter response of retinal arterioles was studied in all groups after an increase in the blood pressure by isometric exercise, during exposition to 8 Hz flickering light, and during simultaneous exposition to both stimulus conditions. RESULTS: The increased blood pressure induced by isometric exercise induced a non-significant vasoconstriction in the normal persons and in the diabetic patients without retinopathy (p=0.10 and p=0.84 respectively), and a non-significant vasodilatation in the diabetic patients with mild retinopathy (p=0.10). The flicker stimulus elicited a significant vasodilatation of retinal arterioles that decreased significantly from the normal persons to the diabetic patients without and with retinopathy (linear regression, p<0.01). The flicker-induced vasodilatation was not significantly affected by a simultaneous increase in the arterial blood pressure in normal persons (p=0.85). Conversely, in the diabetic patients the reduced diameter response during flicker was counteracted by a simultaneous increase in the blood pressure, to a level not differing significantly from the response of normal persons (p=0.75). CONCLUSIONS: Intervention studies aimed at modifying perfusion in retinal disease should consider the interaction between different mechanisms for autoregulating retinal blood flow. New treatment modalities for retinal vascular disease might need to target several mechanisms of tone control in retinal arterioles simultaneously.
BACKGROUND:Diabetic retinopathy is accompanied with changes in the autoregulation of retinal blood flow secondary to changes in the systemic blood pressure and the retinal metabolism. In the present study we tested the working hypothesis that there is an interaction between these mechanisms that might be relevant for understanding and treating flow disturbances in diabetic retinopathy. METHODS: Fifty-four persons divided into three age and sex matched groups were studied: Group 1: twenty normal persons. Group 2: fourteen patients with type 2 diabetes mellitus and no diabetic retinopathy. Group 3: twenty type 2 diabeticpatients with minimal diabetic retinopathy and a diabetes duration similar to that of the patients in group 2. Using the Retinal Vessel Analyzer (RVA) the diameter response of retinal arterioles was studied in all groups after an increase in the blood pressure by isometric exercise, during exposition to 8 Hz flickering light, and during simultaneous exposition to both stimulus conditions. RESULTS: The increased blood pressure induced by isometric exercise induced a non-significant vasoconstriction in the normal persons and in the diabeticpatients without retinopathy (p=0.10 and p=0.84 respectively), and a non-significant vasodilatation in the diabeticpatients with mild retinopathy (p=0.10). The flicker stimulus elicited a significant vasodilatation of retinal arterioles that decreased significantly from the normal persons to the diabeticpatients without and with retinopathy (linear regression, p<0.01). The flicker-induced vasodilatation was not significantly affected by a simultaneous increase in the arterial blood pressure in normal persons (p=0.85). Conversely, in the diabeticpatients the reduced diameter response during flicker was counteracted by a simultaneous increase in the blood pressure, to a level not differing significantly from the response of normal persons (p=0.75). CONCLUSIONS: Intervention studies aimed at modifying perfusion in retinal disease should consider the interaction between different mechanisms for autoregulating retinal blood flow. New treatment modalities for retinal vascular disease might need to target several mechanisms of tone control in retinal arterioles simultaneously.
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