Early Decrease of Skin Blood Flow in Response to Locally Applied Pressure in Diabetic Subjects

Abstract

Pressure ulcers are common debilitating complications of diabetes that are caused by tissue ischemia. Skin blood flow in response to locally applied pressure might be impaired in diabetic patients because of the combined effects of a typically low skin temperature and alterations in microcirculatory function, and could be worsened by neuropathy. We measured skin blood flow by laser Doppler flowmetry over the internal anklebone in response to local pressure applied at 5.0 mmHg/min in three groups of diabetic patients (with clinical and subclinical neuropathy and without neuropathy) and in healthy matched control subjects at usual room temperature. Compared with in matched control subjects with comparable skin temperatures (29.3 ؎ 0.4 vs. 28.7 ؎ 0.4°C), in diabetic patients the skin blood flow response to locally applied pressure was further impeded, even in those without neuropathy. Indeed, skin blood flow decreased significantly from baseline at much lower applied pressure (7.5 mmHg) in diabetic subjects, again even in those without neuropathy, than in control subjects (48.8 mmHg). The large difference between these pressures could partially explain diabetic patients' high risk of developing decubitus and plantar ulcers. Diabetes 51:1214 -1217, 2002 P ressure ulcers are common debilitating complications of diabetes (1). Diabetes disturbs the autonomic regulation of skin microcirculation, even in the absence of neuropathy. Moreover, sensory diabetic neuropathy mainly affects unmyelinated primary afferent fibers (2) and impairs the vasodilation related to normally functioning unmyelinated C fibers (3,4). We recently reported on cutaneous pressure-induced vasodilation (PIV) in humans (5,6) and rats (7) as a physiological response to an increase in nonnoxious progressive local pressure. This mechanism allows skin blood flow to increase in response to locally applied pressure, whereas in its absence, skin blood flow is progressively decreased with application of increased local pressure. Although it results from nonpainful stimulation, this mechanism has been shown to disappear after chronic treatment with capsaicin in animals and humans (5,7), suggesting that it is dependent on the normal function of capsaicin-sensitive primary nervous afferents. Because temperature and blood flow in cutaneous microcirculation are highly correlated (8), skin temperature may have a major effect on skin blood flow response to applied pressure. Therefore, we hypothesized that the skin blood flow response to locally applied pressure would be impaired in diabetic patients because of the combined effects of their typically low skin temperature and diabetes-induced alterations of the vascular and nervous systems. To verify this hypothesis, we measured the effects of locally applied pressure on skin blood flow over the internal anklebone in diabetic patients with clinically apparent or subclinical neuropathy and without neuropathy and in healthy matched control subjects at usual ambient temperature. RESEARCH DESIGN AND METHODSSubjects. Subj...

Early Endothelial Dysfunction Severely Impairs Skin Blood Flow Response to Local Pressure Application in Streptozotocin-Induced Diabetic Mice

“…In a previous study, we reported an early decrease of skin blood flow at low applied pressures in diabetic patients both with and without clinical neuropathy, compared with control subjects (3). In the present study, we observed an early decrease in LDF in response to external pressure application in the diabetic group that is similar to the one observed by Fromy et al (3) in diabetic patients compared with control subjects. Indeed, LDF in 1-week diabetic mice was reduced beginning at a pressure as mild as 0.46 kPa, whereas LDF in control mice was not reduced until higher pressures (1.16 kPa).…”

Impaired Pressure-Induced Vasodilation at the Foot in Young Adults With Type 1 Diabetes

“…Therefore, we speculated that the PIV, relying on unmyelinated afferent excitation, could be a missing link between neuropathy and foot ulcer in diabetes. We previously showed that skin blood flow in response to locally applied pressure is impeded in diabetic patients compared with control subjects at comparable, relatively low skin temperature (8). However, in this study, we did not observe PIV at the foot level in healthy subjects.…”

Diabetic foot ulceration and amputation

“…Impaired vasodilatory response to plantar pressure causing tissue ischemia is the common final pathway, according to various theories, of the development of diabetic foot ulcers (Boulton et al, 2000). Diabetic patients (with or without peripheral neuropathy) suffer from various forms of microvascular dysfunction, including abnormal vasomotion (Benbow et al, 1995;Stansberry et al, 1996;Bernardi et al, 1997), impaired vasodilatory response to local heating (Malik et al, 1993;Stansberry et al, 1999), decreased blood flow under or after pressure loading (Fromy et al, 2002;Koitka et al, 2004), endothelial nitric oxide dysfunction (Veves et al, 1998), and attenuated response to sympathetic maneuvers (Aso et al, 1997).…”