The development of diabetic retinopathy is a major concern in the management of diabetes mellitus. Previous research into this complication, using techniques such as fluorescein angiography [1] and Laser Doppler velocimetry [2±5], has contributed to the understanding of the process and progression of retinopathy [2, 4±7].Clinical studies have shown that ocular haemodynamic changes in diabetes are complex and still have to be fully defined. Generally an initial reduction in retinal blood flow velocity has been observed in the early stages of diabetes before the onset of any clinically recognisable retinopathy [4,5,7,9,10]. A positive transition is then seen as retinal blood speed in- Diabetologia (2001) Abstract Aims/hypothesis. This study investigated the influence of plasma glucose upon pulsatile ocular blood flow in subjects with Type II (non-insulin-dependent) diabetes mellitus. Methods. A total of 19 subjects with Type II diabetes and 8 normal control subjects undertook a meal tolerance test after an overnight fast. The pulsatile ocular blood flow, using the Ocular Blood Flow Tonometer, and plasma glucose concentrations were taken at times 0 min, 90 min and 240 min. Blood pressure and glycated haemoglobin concentrations, in the subjects with diabetes, were also measured at time 0 min. Pulsatile ocular blood flow and plasma glucose were also measured at times 0 and 90 min in 5 subjects with Type II diabetes mellitus who remained fasting.Results. It was found that the subjects with diabetes who undertook the meal tolerance test showed a significant increase in both plasma glucose concentrations and pulsatile ocular blood flow from time 0±90 min, followed by a decrease from 90 min to the end of the session at 240 min. (p < 0.001 in each case). Regression analysis showed a significant correlation between the change in pulsatile ocular blood flow and the change in plasma glucose concentration (r = 0.671, p = 0.001). Control subjects showed no significant change in either plasma glucose or pulsatile ocular blood flow during the meal tolerance test. Subjects with diabetes mellitus who remained fasting also showed no significant change in pulsatile ocular blood flow or plasma glucose concentrations. No correlation was found between glycated haemoglobin concentrations or blood pressure and pulsatile ocular blood flow. Conclusion/interpretation. Pulsatile ocular blood flow is influenced by changes in plasma glucose concentrations in Type II diabetes mellitus, indicating that uncontrolled hyperglycaemia might result in a higher pulsatile ocular blood flow than might otherwise be expected. [Diabetologia (2001) 44: 700±705]

Summed OP amplitudes, which are known to reflect the efficiency of the retinal circulation, increased with elevated plasma glucose. This effect was not immediately reversible. Latencies appear not to be affected.

Purpose:  Our aim was to determine if pulsatile ocular blood flow (POBF) measurements could distinguish between type 2 diabetes mellitus (DM) subjects with and without diabetic retinopathy (DR). Methods:  Ninety‐eight DM subjects were recruited. POBF was measured using an Ocular Blood Flow tonometer and retinopathy was assessed using retinal digital photography. The duration of diabetes, blood pressure, glycosylated haemoglobin and plasma glucose level were also recorded. Results:  Seventy‐two subjects had no DR and 26 subjects exhibited mild to moderate non‐proliferative DR. POBF was higher in those subjects with non‐proliferative DR but did not reach significance. Those subjects receiving insulin treatment had a significantly longer duration of DM, higher HbA1c and plasma glucose levels and greater incidence of non‐proliferative DR compared to subjects receiving oral hypoglycaemic agents, who in turn demonstrated higher levels of these parameters than those who were controlled by diet alone (ANOVA p < 0.05 in all cases). POBF was found to increase with level of management but not significantly so. Conclusions:  A single measurement of POBF does not distinguish between subjects with and without mild/moderate non‐proliferative DR.