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J Appl Physiol (October 6, 2005). doi:10.1152/japplphysiol.00943.2005
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Submitted on August 2, 2005
Accepted on September 30, 2005

Delayed threshold for active cutaneous vasodilation in patients with type 2 diabetes mellitus

Diane E. Wick1, Shelly K. Roberts2, Ananda Basu3, Paola Sandroni4, Robert D. Fealey4, David Sletten4, and Nisha Charkoudian1*

1 Department of Physiology and Biomedical Engineering, Mayo Clinic College of Medicine, Rochester, MN, USA; Department of Anesthesiology, Mayo Clinic College of Medicine, Rochester, MN, USA
2 Department of Physiology and Biomedical Engineering, Mayo Clinic College of Medicine, Rochester, MN, USA
3 Department of Endocrinology, Mayo Clinic College of Medicine, Rochester, MN, USA
4 Department of Neurology, Mayo Clinic College of Medicine, Rochester, MN, USA

* To whom correspondence should be addressed. E-mail: charkoudian.nisha{at}mayo.edu.

Epidemiological evidence suggests decreased heat tolerance in patients with type 2 diabetes mellitus (T2DM), but it is not known whether the mechanisms involved in thermoregulatory control of skin blood flow are altered in these patients. We tested the hypothesis that individuals with T2 DM have a delayed internal temperature threshold for active cutaneous vasodilation during whole body heating compared to healthy control subjects. We measured skin blood flow using laser Doppler flowmetry (LDF), internal temperature (TOR) via sublingual thermocouple, and mean arterial pressure via Finometer at baseline and during whole body heating in 9 T2DM patients and 10 control subjects of similar age, height and weight. At one LDF site sympathetic noradrenergic neurotransmission was blocked by local pretreatment with bretylium (BT) to isolate the cutaneous active vasodilator system. Whole body heating was conducted using a water-perfused suit. There were no differences in pre-heating internal temperature between groups (p > 0.10). Patients with T2 DM exhibited an increased internal temperature threshold for the onset of vasodilation at both untreated and BT-treated sites. At BT-treated sites, TOR thresholds were 36.28 ± 0.07 °C in controls and 36.55 ± 0.05 °C in T2 DM patients (p < 0.05), indicating delayed onset of active vasodilation in patients. Sensitivity of vasodilation was variable in both groups, with no consistent difference between groups (p > 0.05). We conclude that altered control of active cutaneous vasodilation may contribute to impaired thermoregulation in patients with T2 DM.




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