Reduction of 0.1 Hz microcirculatory fluctuations as evidence of sympathetic dysfunction in insulin-dependent diabetes

Abstract

Objective: Loss of spontaneous fluctuations in resting microcirculatory flow has been described in diabetes mellitus, but its mechanism remains unexplained.

Methods: The autonomic control of forearm skin microcirculation was investigated in 23 insulin-dependent diabetic human subjects (median age 39 years, range 27-50) and in 23 age-matched controls (median age 38 years, range 20-57), by laser-Doppler flowmetry. Using spectral analysis of spontaneous microvascular fluctuations, we measured the power of 0.1 Hz ('10-second rhythm') fluctuations, dependent on sympathetic control, and of respiration-related, high-frequency fluctuations, due to the transmission of mechanical chest activity. Autonomic function abnormalities were assessed by 5 tests of cardiovascular reflexes.

Results: Abnormalities in cardiovascular autonomic tests were present in 7/23 patients: deep breathing was abnormal 4 in patients, standing in 2, handgrip in 3, cross-correlation in 4, and Valsalva ratio in 0. The power of 0.1 Hz microcirculatory fluctuations was significantly lower in diabetic than in control subjects (2.57 +/- 0.16 vs 3.48 +/- 0.09 In-mV2, mean +/- s.e.m., P < 0.001), whereas that of respiratory fluctuations was similar (2.60 +/- 0.24 vs 2.56 +/- 0.19 In-mV2, P = n.s.). The 0.1 Hz power was 2 standard deviations below the mean of controls (P < 0.05) in 13/23 diabetic patients; this abnormality was significantly more frequent than abnormalities in any other autonomic test (P < 0.001).

Conclusions: Since the observed reduction was confined to those microvascular fluctuations under autonomic control, but not to those dependent on passive mechanical transmission, the reduction in spontaneous microcirculatory vasomotion appears to be determined mainly by sympathetic dysfunction. Sympathetic impairment of skin microvascular control seems to be a common finding, and is probably an early index of autonomic dysfunction in insulin-dependent diabetes.