Background— We sought to identify whether transcutaneous oxygen tension (tcP o ₂ ) measurements could be used to noninvasively detect lesions in the arterial network supplying blood flow to the hypogastric circulation. Methods and Results— A study was undertaken in vascular patients with suspected (PC, n=43) and not with suspected (NPC, n=34) proximal ischemia. TcP o ₂ was measured on both buttocks and with a chest reference electrode. Arteriography on the right or left side was positive for stenoses (≥75%) or occlusion of one or more of the following arteries: the aorta, the common iliac arteries, or the internal iliac arteries. The arteriography was compared with the resting tcP o ₂ values (REST) and with the minimal value (MIN) and maximal change from rest normalized to eventual chest changes (DROP) recorded during or after a treadmill test. REST, MIN, and DROP were, respectively, as follows in positive versus negative arteriograms (mean±SD; in mm Hg): 80.2±10.9 versus 78.6±11.5 ( P >0.05), 55.2±20.0 versus 69.9±15.8 ( P <0.001), and −31.8±17.6 versus −9.5±6.4 ( P 0.05), 64.4±21.0 versus 75.1±14.6 ( P <0.02), and −24.1±13.5 versus −8.7±4.8 ( P <0.0001) in NPC. In PC and NPC respectively, with a cutoff point of −16 and −15 mm Hg, DROP showed, respectively, 83%/82% and 79%/86% sensitivity/specificity in the diagnosis of positive arteriograms. Conclusions— Proximal ischemia is a frequent finding in vascular patients. TcP o ₂ measurement on the buttocks during exercise is a sensitive and specific indicator for lesions in the arterial tree toward the hypogastric circulation. Potentially it could objectively assess the response to endovascular or surgical approaches to iliac lesions.

Vascular calcification is a complex and dynamic process occurring in various physiological conditions such as aging and exercise or in acquired metabolic disorders like diabetes or chronic renal insufficiency. Arterial calcifications are also observed in several genetic diseases revealing the important role of unbalanced or defective anti- or pro-calcifying factors. Pseudoxanthoma elasticum (PXE) is an inherited disease (OMIM 264800) characterized by elastic fiber fragmentation and calcification in various soft conjunctive tissues including the skin, eyes, and arterial media. The PXE disease results from mutations in the ABCC6 gene, encoding an ATP-binding cassette transporter primarily expressed in the liver, kidneys suggesting that it is a prototypic metabolic soft-tissue calcifying disease of genetic origin. The clinical expression of the PXE arterial disease is characterized by an increased risk for coronary (myocardial infarction), cerebral (aneurysm and stroke), and lower limb peripheral artery disease. However, the structural and functional changes in the arterial wall induced by PXE are still unexplained. The use of a recombinant mouse model inactivated for the Abcc6 gene is an important tool for the understanding of the PXE pathophysiology although the vascular impact in this model remains limited to date. Overlapping of the PXE phenotype with other inherited calcifying diseases could bring important informations to our comprehension of the PXE disease.

Background— The maximal walking distance (MWD) performed on a treadmill test remains the “gold standard” in estimating the walking capacity of patients who have peripheral arterial disease with intermittent claudication, although treadmills are not accessible to most physicians. We hypothesized that global positioning system (GPS) recordings could monitor community-based outdoor walking and provide valid information on walking capacity in patients with peripheral arterial disease. Methods and Results— We studied 24 patients (6 women) with arterial claudication (median [25th to 75th percentile] values: 57 years old [48 to 67 years], 169 cm tall [164 to 172 cm], weight 81 kg [71 to 86 kg], and ankle-brachial index 0.64 [0.56 to 0.74]). MWD on the treadmill was 184 m (144 to 246 m), which was compared with the results of self-reported MWD, the distance score from the Walking Impairment Questionnaire, MWD observed during a 6-minute walking test, and MWD measured over a GPS-recorded unconstrained outdoor walk in a public park. Self-reported MWD, Walking Impairment Questionnaire distance score, 6-minute walking test score, and GPS-measured MWD were 300 m (163 to 500 m), 28% (15% to 47%), 405 m (338 to 441 m), and 609 m (283 to 1287 m), respectively. The best correlation with MWD on the treadmill test was obtained with the MWD measured by the GPS (Spearman r =0.81, P <0.001). Conclusions— Outdoor walking capacity measured by a low-cost GPS is a potentially innovative way to study the walking capacity of patients with peripheral arterial disease. It opens new perspectives in the study of walking capacity for vascular patients with claudication under free-living conditions or for physicians who do not have a treadmill.

The vasodilatation resulting from prolonged square‐wave monopolar current application as used in iontophoresis is assumed to rely on an axon reflex. Involvement of prostaglandins in the anodal current‐induced vasodilatation remains unclear. We tested the hypothesis that prostaglandins participate in a sensitisation mechanism to current application rather than as direct vasodilators. In healthy volunteers, laser Doppler flowmetry (LDF) was recorded in the forearm during and following isolated or repeated 0.1 mA transcutaneous anodal current applications, using deionised water as a vehicle. Segmented current applications of 6 or 12 mC resulted in an LDF increase twice that observed following current applications of comparable total charge delivered all at once (P < 0.05). Following a 1 min anodal application, a slow and prolonged LDF drift occurred (slope: 0.3 ± 0.5 arbitrary units min⁻¹). When the same current application was repeated after intervals of 5 and 20 min, an abrupt vasodilatation occurred, with maximal LDF amplitude of 53.5 ± 34.0 and 48.2 ± 19.1 arbitrary units, respectively. Pretreatment with 1 g oral aspirin abolished the abrupt vasodilatation to repeated current application but not the initial slow drift. We suggest that vasodilatation occurs through two parallel pathways: (1) a slow progressive drift of LDF of limited amplitude insensitive to aspirin pretreatment, and (2) an abrupt vasodilatation probably resulting from afferent fibre activation, appearing if a preliminary sensitisation by current application is performed. Sensitisation lasts for at least 20 min, and is blocked by aspirin, suggesting participation of prostanoids.

The participation of prostaglandins (PGs) in the cutaneous vasodilatation to acetylcholine (ACh) applied via iontophoresis is under debate. Using laser Doppler flowmetry, we studied the long lasting effect (20 min) of iontophoretic application (30 s; 0.1 mA) of ACh on the human forearm. Experiments were repeated (1) using deionized water instead of ACh to test the effect of current application, (2) after scopolamine treatment to inhibit muscarinic cholinergic receptors, and (3) 2 h, 3 days and 10 days following inhibition of PG synthesis with aspirin or a placebo control. Cutaneous vascular conductance (CVC) was calculated at rest (CVC_rest), at peak vasodilatation in the first 5 min following ACh iontophoresis (CVC_peak), and 20 min after iontophoresis (CVC₂₀). The minimal CVC (CVC_min) following iontophoresis was also determined. Cutaneous response to ACh displayed a biphasic pattern with an early and transient peak (CVC_peak: 62 ± 8% of the maximal CVC induced by local heating (MVC)) followed by a long lasting slower vasodilatation (CVC_min: 44 ± 6; CVC₂₀: 56 ± 5%MVC). The current itself had no major effect. Scopolamine almost abolished both phases. The long lasting phase was aspirin sensitive but not the transient phase. At hour 2 post‐aspirin, CVC_peak was 61 ± 10, CVC_min 26 ± 6 and CVC₂₀ 29 ± 6%MVC. At day 3, CVC_peak was 53 ± 9, CVC_min 22 ± 3 and CVC₂₀ 25 ± 4%MVC. At day 10, CVC_peak was 67 ± 10, CVC_min 47 ± 7 and CVC₂₀ 50 ± 8%MVC. Placebo had no effect. We conclude that PGs participate in the vasodilator response following ACh iontophoresis. Previous non‐steroidal anti‐inflammatory drug treatments must be taken into account when studying the effect of ACh iontophoresis.