In some patients with type 1 diabetes, various physiologic reactions during a cold pressor test (CPT) are impaired. Whether this is caused by diabetic autonomic neuropathy, disturbed secretion of catecholamines, or disturbed blood glucose control is unknown. The authors, therefore, performed CPTs in patients with type 1 diabetes and in control subjects. They measured blood glucose concentrations, insulin concentrations, cardiac autonomic reflexes, and (before and after the CPT) venous catecholamine concentrations and analyzed correlations between these variables. Twenty-two patients with type 1 diabetes (17 men, 5 women; mean age +/- SD, 26.6 +/- 6.5 y; diabetes duration, 7.6 +/- 0.7 y; glycosylated hemoglobin concentration, 7.7 +/- 2.4%) and 35 control subjects with comparable age and gender distributions were studied. Venous catecholamines were measured before and at the end of a 5-minute CPT. In patients with diabetes, only noradrenaline concentrations increased during the CPT, whereas adrenaline concentrations that were already increased at rest did not change. Adrenaline concentrations correlated inversely with insulin concentrations. In control subjects, both adrenaline and noradrenaline increased significantly during the CPT. In both groups, the magnitude of the individual change in catecholamine concentrations was inversely correlated with the respective resting concentration. Changes in catecholamines, cardiovascular reflex tests, and blood glucose concentrations did not correlate with blood pressure changes. The authors conclude that, in patients with diabetes, resting adrenaline concentrations are related to insulin concentrations. Contrary to control subjects, in patients with diabetes, only noradrenaline increased during CPTs. In both groups, changes in catecholamine concentrations after the CPT were inversely related to the respective resting concentrations.
Microcirculatory changes occur early in insulin-dependent diabetes mellitus (IDDM) and are believed to be an early feature of late diabetic complications, leading to reduced oxygen pressure and hypoxia in the skin and other tissues. Whether muscle oxygen supply is also altered is unknown. Therefore, the authors analyzed polarographic measurements of muscle oxygen tension in 44 healthy type I diabetic patients (mean age 28 years; mean diabetes duration 7 years) and in 57 healthy controls, matched for age, sex, and body mass index, and the corresponding influencing factors. Two measurements were taken at rest 60 minutes apart in the anterior tibial muscle. Muscle oxygen tensions did not differ between IDDM patients and controls (23.0 +/- 8.6 vs 25.3 +/- 9.0 mmHg) and were reproducible on repeated measurements (25.3 +/- 9.7 vs 25.5 +/- 7.4 mmHg). Coefficients of variation were 13.5 +/- 10.8% in IDDM patients and 13.1 +/- 9.3% in controls. Compared with controls, in IDDM patients hemoglobin A1c (HbA1c) and blood glucose concentrations were elevated, and arterial oxygen pressure was significantly lower. Muscle oxygen tensions were positively correlated with blood glucose concentrations in IDDM patients (Rho=0.48, P=0.002) but not with HbA1c or with insulin concentrations. The authors conclude that the polarographic measurement of muscle oxygen tension is a reliable method with good reproducibility. Hypoxia in the anterior tibial muscle of type I diabetic patients can be excluded. In IDDM patients the level of muscle oxygen tension is correlated with the level of blood glucose concentration.
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