Early detection of vascular dysfunction in type I diabetes.

Blood flow and transcutaneous oxygen tension was measured by venous occlusion plethysmography and a transcutaneous oxygen electrode before and after 5 min of arterial occlusion in the forearm of young adult subjects with type I (insulin-dependent) diabetes without overt evidence of angiopathy. In control subjects (n = 21), the forearm blood flow increased by greater than or equal to 2.8-fold at 30 s after ischemia. Diabetic subjects with glycosylated hemoglobin (GHb) less than or equal to 9.5% (n = 15) exhibited a blood flow response that was not statistically different from normal control subjects. Diabetic subjects with GHb greater than or equal to 12.5% (n = 23) did not exhibit an increase in the postischemic blood flow. When blood flow patterns for the first 14 diabetic subjects were examined regardless of GHb value, four patterns of response were noted: 1) normal pattern (n = 3), 2) normal postischemic rise in blood flow with a prolonged elevation (n = 3), 3) no postischemic rise (n = 4), and 4) variable baseline blood flow with a decrease in blood flow postischemia (n = 4). This approach indicated that a comparison of means obscured potentially meaningful abnormal patterns. Abnormalities in the response of the transcutaneous oxygen tension to ischemia were observed in both groups of diabetic patients, but the difference between diabetic patients in good and poor control was less obvious. We have defined an abnormal response of blood flow and transcutaneous oxygen tension to ischemia that may correlate to glycemic control and have identified several patterns of blood flow after ischemia that may be important in defining the etiology and natural history of diabetic angiopathy.