Impairment of cutaneous arteriolar 0.1 Hz vasomotion in diabetes.

Arteriolar vasomotion, the cyclic contraction/dilation of terminal arterioles, is disordered in diabetes. The aim of the present study was to characterize the impairment of cutaneous vasomotion in type 1 and type 2 diabetes, especially with regard to the influence of metabolic control and to the response to shear stress. Twenty type 1 and 23 type 2 diabetic patients were investigated. Vasomotion waves were recorded in single capillaries at the dorsal middle phalangeal area of the left ring finger during rest, after warming the skin temperature to 33 degrees C, and after 3-min arterial occlusion by means of laser Doppler anemometry. Suprasystolic occlusion caused an increase in amplitudes of vasomotion only in type 1 diabetic patients (0.12 +/- 0.04 mm/s vs. 0.36 +/- 0.06 mm/s, p = 0.001). In type 1 but not in type 2 diabetic patients, both systolic and diastolic blood pressure correlated positively with amplitudes of resting vasomotion (r = 0.62, p = 0.002 and r = 0.65, p = 0.001, respectively). Amplitudes of vasomotion after warming up at frequencies of 5 - 8 cycles per minute (0.08 - 0.13 Hz) correlated inversely with the levels of glycated hemoglobin (HbA 1c ) (r = - 0.56, p = 0.005) only in type 1 diabetic patients. In conclusion, we found suprasystolic occlusion and increasing blood pressure to provoke vasomotion with a concomitant decrease in effective vascular resistance only in type 1 diabetic patients. The impaired vasomotion response to shear stress in type 2 diabetes might favour the development of skin lesions and arterial hypertension. Insufficient glycemic control seems to be an important factor in the pathogenesis of impaired vasomotion in type 1 diabetes.

Impaired 0.1-Hz vasomotion assessed by laser Doppler anemometry as an early index of peripheral sympathetic neuropathy in diabetes.

Impairment of 0.1-Hz vasomotion, which was found in diabetic patients, was suggested to be an early index of sympathetic dysfunction. We studied the relationships between alterations in vasomotion and both cardiac autonomic and sensory neuropathy. Twenty type 1 and 22 type 2 diabetic patients were investigated. Vasomotion was recorded in single capillaries at the dorsal middle phalangeal area of the left ring finger by means of laser Doppler anemometry. Cardiac autonomic neuropathy was assessed by spectral analysis of heart rate variation during rest and recording heart rate responses to deep breathing and Valsalva manoeuvre. Sensory neuropathy was investigated by measuring heat pain, vibration, and thermal sensory thresholds. Impaired vasomotion was more often (82.4%) found in diabetic patients with at least one altered cardiac autonomic test, but also in 47.1% of those with all of these tests being normal (P = 0.035). Both heart rate variation coefficient during rest (r = 0.40, P = 0.045) and Valsalva ratio (r = 0.41, P = 0.037) correlated positively with amplitudes of vasomotion in type 1 diabetic patients. The prevalence of impaired vasomotion was not higher in patients with sensory neuropathy compared to those with normal sensory functions. A disturbed warm sensation was only found in 2 patients and none had an abnormal heat pain threshold. Our data indicate that impairment of 0.1-Hz vasomotion precedes parasympathetic neuropathy, assessed by heart rate variation tests, and abnormalities in warm and heat pain sensation. Reduction of arteriolar vasomotion, detected by laser Doppler anemometry, might be an early index of sympathetic dysfunction, because it correlates with disturbances in those cardiac autonomic tests, which are at least in part under sympathetic control.