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

Abstract

Vascular and neurological mechanisms are both likely to be involved in foot ulcer. We recently reported a pressure-induced vasodilation (PIV), relying on unmyelinated afferent excitation. We previously found that cutaneous blood flow in response to locally applied pressure might be impaired in diabetic patients because of the combined effects of low cutaneous temperature and alterations in microcirculatory function. Therefore, we aimed to analyze whether, at a relatively high cutaneous temperature, PIV is present in type 1 diabetes and to assess endothelial-dependent vasodilation and endothelium-independent vasodilation. We measured cutaneous blood flow using laser Doppler flowmetry on the head of the first metatarsus in response to applied pressure at 5.0 mmHg/min in warm conditions (29.5 ؎ 0.2°C). Responses to iontophoresis of acetylcholine (endothelium dependent) and sodium nitroprusside (endothelium independent) were measured using laser Doppler flowmetry in the forearm. The data indicate that PIV exists at the foot level in normal subjects, whereas it was not found in diabetic patients. In diabetic patients, the nonendothelial-mediated response to sodium nitroprusside was preserved, whereas the endothelial-mediated response to acetylcholine was impaired. These findings might be relevant to the high prevalence of foot ulcer that occurs in diabetic patients. Diabetes 53: [721][722][723][724][725] 2004

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

“…These results are in accordance with those obtained in diabetic patients (40). These findings point out that PIV response seems to be highly sensitive to endothelial NO levels, and therefore endothelial impairment by itself is sufficient to alter severely the PIV response.…”

Evaluation of Repositioning in Pressure Ulcer Prevention

“…Previous studies of PIV have used LDF, and by using the same measurement technique the results are easier to compare (Abraham et al, 2001;B. Fromy et al, 2010;Koïtka et al, 2004). The baseline threshold was chosen based on a previous study by Sanada et al (1997) who showed that patients who had an inability to increase blood flow over baseline values during long pressure exposures were the ones who tended to develop pressure ulcers.…”

“…The absence of PIV leads to a decrease in blood flow even in response to low levels of pressure, and this makes the individual vulnerable to externally applied pressure. The PIV function has been shown to be altered in diabetic patients (Koïtka et al, 2004) and in the elderly Fromy et al, 2010), but a lack of PIV response can also be found in young, healthy individuals . With progressively increasing pressure to the skin, the PIV response has been shown to reach its maximum at pressure levels of 25-50 mmHg in young, healthy individuals (Fromy et al, 2010;Schubert & Fagrell, 1989).…”

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).…”