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External iliac artery endofibrosis is a rare disease affecting mainly highly trained cyclists. As the disease has only recently been described, the long term spontaneous evolution of external iliac artery endofibrosis is not known. We report a suspected case of forty-year spontaneous evolution of endofibrosis in a former competition cyclist. The results of this isolated original report suggest, as we intuitively presumed, that the lesions may stabilise when intensive training is stopped. Therefore, when no symptoms are noted on usual daily activity or submaximal exercise, surgery should not be performed. Surgery should only be considered, at the request of the subjects to allow them to continue competing. [ABSTRACT FROM AUTHOR]

Although recent studies have compared the effect of progressive exercise tests to constant moderate work load tests on ankle systolic blood pressure (ASBP) and ankle to arm index (AAI) in claudicants, little is known about the relation of ASBP and AAI to work load in healthy young men. Fifteen normal volunteers were asked to cycle 40, 60, 80 100% of VO(2max). Ankle and humeral pressures were recorded simultaneously, at rest and 1 minute after the end of each test. Thereafter, AAI was calculated as the ratio of ankle to humeral systolic pressure. Compared to resting values: 134.8+/-13.9 mmHg, ASBP increased significantly following sub maximal tests up to 157.8+/-28.1 mmHg (p<0.005), but was not increased following maximal exercise: 141.5+/-28.2 mmHg (NS). On the other hand, AAI showed a progressive decrease from 1.14+/-0.06 at rest to 1.06+/-0.08 (p<0.005), to 0.98+/-0.07 (p<0.005), to 0.84+/-0.06 (p<0.005) and to 0.75+/-0.09 (p<0.005) following 40, 60, 80 and 100% of VO(2max) respectively. In summary, AAI following exercise is inversely related to workload whereas ASBP is not. We suggest that when studying ankle systolic blood pressure response to heavy load exercises, results should always be compared to humeral pressure, and expressed as ankle to arms indexes. [ABSTRACT FROM AUTHOR]

Diabetic foot ulcer (DFU) is a problem worldwide, and prevention is crucial. We hypothesized that the inability of the skin to respond to pressure is involved in DFU pathogenesis and could be an important predictive factor to take into account. We included 29 patients with DFU and 30 patients with type 2 diabetes without DFU. Neuropathy and skin blood flow at rest were assessed in response to acetylcholine, sodium nitroprusside, local heating (42°C), and to nonnoxious locally applied pressure. Results were compared with those obtained from 10 healthy age-matched control subjects. Vasodilatation in response to pressure was significantly impaired in both groups with diabetes compared with healthy subjects. The vasodilator capacity to pressure was significantly lower in patients with DFU compared with those without DFU, despite the absence of significant difference in cutaneous pressure perception threshold and vascular reactivity to acetylcholine, sodium nitroprusside, and heat. This pronounced alteration of neurovascular response to pressure in patients with DFU is a good marker of skin vulnerability and could be used to better predict individuals at risk., (© 2019 by the American Diabetes Association.)

Nerve recovery following injury is usually incomplete, leaving functional deficits. Our aim was to investigate the neural changes in pro-angiogenic, pro-inflammatory and apoptotic factors during and after chronic nerve compression (CNC). Nerve function was impaired after CNC and was progressively restored after nerve decompression, while nerve blood flow was elevated. While the expression of the pro-inflammatory and pro-angiogenic cytokines IL-6, TNF-α and VEGF-A was high during and after CNC, we observed that inhibition of VEGF-A receptors strongly counteracted the angiogenic response induced by the ex vivo CNC. Activation of the pro-survival transcription factor nuclear factor-kappa B (NF-κB) increased during CNC, returning to control levels after nerve decompression. After nerve decompression, the downregulation of Mdm2 correlated well with an increased expression of pro-apoptotic transcription factor p53. All together, we bring novel evidence that CNC activates transcription factors such as NF-κB and p53, which are key effectors of the cellular stress response, suggesting a neuroprotective process associated with an increased VEGF-A-mediated neurotrophic effect. Our results highlight the role of pro-angiogenic and pro-inflammatory cytokines during CNC that are reinforced by increasing neurotrophic capacity during recovery to promote nerve regeneration.

With advancing age, a decline in the main sensory modalities including touch sensation and perception is well reported to occur. This review mainly outlines the peripheral components of touch perception highlighting ageing influences on morphological and functional features of cutaneous mechanical transducers and mechanosensitive ion channels, sensory innervation, neurotransmitters and even vascular system required to ensure efferent function of the afferent nerve fibres in the skin. This, in conjunction with effect of ageing on the skin per se and central nervous system, could explain the tactile deficit seen among the ageing population. We also discuss appropriate tools and experimental models available to study the age-related tactile decline., (Copyright © 2013 Elsevier B.V. All rights reserved.)

Pressure-induced vasodilation (PIV) delays the decrease in cutaneous blood flow produced by local application of low pressure to the skin, a physiologically appropriate adjustment of local vasomotor function. Individuals without a normal PIV response have a high risk of ulceration. Here we demonstrate that acid-sensing ion channel 3 (Asic3) is an essential neuronal sensor for the vasodilation response to direct pressure in both humans and rodents and for protecting against pressure ulcers in mice.

Most studies of chronic nerve compression focus on large nerve function in painful conditions, and only few studies have assessed potential changes in the function of small nerve fibers during chronic nerve compression and recovery from compression. Cutaneous pressure-induced vasodilation is a neurovascular phenomenon that relies on small neuropeptidergic fibers controlling the cutaneous microvasculature. We aimed to characterize potential changes in function of these small fibers and/or in cutaneous microvascular function following short-term (1-month) and long-term (6-month) nerve compression and after release of compression (ie, potential recovery of function). A compressive tube was left on one sciatic nerve for 1 or 6 months and then removed for 1-month recovery in Wistar rats. Cutaneous vasodilator responses were measured by laser Doppler flowmetry in hind limb skin innervated by the injured nerve to assess neurovascular function. Nociceptive thermal and low mechanical thresholds were evaluated to assess small and large nerve fiber functions, respectively. Pressure-induced vasodilation was impaired following nerve compression and restored following nerve release; both impairment and restoration were strongly related to duration of compression. Small and large nerve fiber functions were less closely related to duration of compression. Our data therefore suggest that cutaneous pressure-induced vasodilation provides a non-invasive and mechanistic test of neurovascular function that gives direct information regarding extent and severity of damage during chronic nerve compression and recovery, and may ultimately provide a clinically useful tool in the evaluation of nerve injury such as carpal tunnel syndrome., (Copyright © 2011 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.)

Changes in chest transcutaneous-pO(2) at rest (ΔtcpO(2)) mimic absolute changes in arterial-pO(2) during moderate exercise, although the absolute starting values may dramatically differ. We retrospectively studied 485 patients (group 1), prospectively studied 292 new patients (group 2) and estimated the intra-test and the test-retest reproducibility of ΔtcpO(2) during constant-load treadmill tests: 3.2 km h(-1), 10% grade, using the cross correlation technique. Patients were classified into groups according to their best fit to nine pre-defined mathematic models. Respectively, 71% and 76% of patients of groups 1 and 2 fitted with a model showing a ΔtcpO(2) increase during and a decrease following exercise. Another 18% and 12% of the patients of groups 1 and 2 respectively fitted with a model that showed an abrupt decrease at exercise onset, a slow increase during walking and an overshoot in the recovery period, referred here as a walking-induced transcutaneous hack (WITH) profile. The mean r(max) value for the cross-correlation analysis was 0.919 ± 0.091 and 0.800 ± 0.129 for intra-test and test-retest reproducibility. Most profiles show the expected ΔtcpO(2) exercise-induced increase. Future studies are needed to confirm and explain the WITH profiles that we found, and screen for potential-associated diseases.

In endothelial function, prostacyclin (PGI(2)) is as important as nitric oxide (NO); however, no test assesses specifically the vascular function of endogenous PGI(2). We hypothesized that PGI(2) has a dominant role in cathodal current-induced vasodilation (CIV) described in human skin. We thus aimed to study, in physiological conditions, the PGI(2) involvement in cathodal CIV in rats in order to use pharmacological blockers that could not be used in humans. CIV was reduced by cyclooxygenase (COX)-1 and PGI(2) synthase (PGIS) and PGI(2) receptor (IP) blockers, but was unchanged by COX-2 and NO synthase (NOS) blockers. The level of 6-ketoPGF(1)(α) present in skin biopsies, measured as endogenous PGI(2), was increased by cathodal current stimulation, except under COX-1 and PGIS inhibition. This study provides evidence that cathodal CIV mainly relies on the release of PGI(2) endogenously produced through the COX-1/PGIS pathway, and then acts on IP receptors to relax the cutaneous microvessels in healthy rats. In contrast, neither COX-2 nor NOS is involved in CIV and the endogenous PGI(2) release by current stimulation. This finding shows that cathodal current stimulation could be a valuable method to assess the vascular function of endogenous PGI(2) in healthy skin.

Objective: Global positioning system (GPS) recordings can provide valid information on walking capacity in patients with peripheral arterial disease (PAD) and intermittent claudication (IC) during community-based outdoor walking. This study used GPS to determine the variability of the free-living walking distance between two stops (WDBS), induced by lower-limb pain, which may exist within a single stroll in PAD patients with IC and the potential associated parameters obtained from GPS analysis., Methods: This cross-sectional study of 57 PAD patients with IC was conducted in a university hospital. The intervention was a 1-hour free-living walking in a flat public park with GPS recording at 0.5 Hz. GPS-computed parameters for each patient were WDBS, previous stop duration (PSD), cumulated time from the beginning of the stroll, and average walking speed for each walking bout. The coefficient of variation of each parameter was calculated for patients with the number of walking bouts (N(WB)) >or=5 during their stroll. A multivariate analysis was performed to correlate WDBS with the other parameters., Results: Mean (SD) maximal individual WDBS was 1905 (1189) vs 550 (621) meters for patients with N(WB) <5 vs N(WB) >or= 5, respectively (P < .001). In the 36 patients with N(WB) >or= 5, the coefficient of variation for individual WDBS was 43%. Only PSD and cumulated time were statistically associated with WDBS in 16 and 5 patients, respectively., Conclusions: A wide short-term variability of WDBS exists and likely contributes to the difficulties experienced by patients with IC to estimate their maximal walking distance at leisurely pace. Incomplete recovery from a preceding walk, as estimated through PSD, seems to dominantly account for the WDBS in patients with IC.

Healthy skin is protected from pressure-induced ischemic damage because of the presence of pressure-induced vasodilation (PIV). PIV relies on small sensory nerve fibers and endothelial function. Since aging alters both nervous and vascular functions, we hypothesized that PIV is altered with aging. We compared PIV in non-neuropathic and neuropathic older subjects (60-75 years) with that of young subjects (20-35 years). Laser Doppler flowmetry was used to evaluate the cutaneous responses to local pressure application, acetylcholine, and local heating. Quantitative sensory tests were used to evaluate sensory-nerve-fiber function. The non-neuropathic older subjects had an impaired PIV (12+/-7% increase in blood flow with pressure) compared with young subjects (62+/-4%, P<0.001). In the presence of peripheral neuropathy, the older subjects were totally deprived of PIV, leading to early pressure-induced cutaneous ischemia (-31+/-10%, P<0.001). This inability of the skin to adapt to localized pressure in older subjects is related to the severity of the sensory-fiber dysfunction rather than to endothelial dysfunction, which was comparable between the non-neuropathic (141+/-19% increased blood flow with acetylcholine, P<0.05) and neuropathic older subjects (145+/-28% increase, P<0.05) compared with young subjects (234+/-25% increase).

Proximal claudication remains a difficult diagnosis. The ankle to brachial index may be insensitive in the case of isolated hypogastric lesions. Penile pressure represents an alternative method for proximal arteries. Surprisingly, the accuracy of penile pressure measurement in detecting lesions on the arteries supplying pelvic circulation in patients suffering claudication has rarely been studied. We aimed to evaluate the diagnostic accuracy of the penile brachial index < 0.60 (penile over brachial systolic pressure ratio) to non-invasively investigate arteriographic lesions on arteries supplying the hypogastric circulation in 88 male patients referred for Fontaine stage II. The receiver operating characteristic (ROC) curve was used to define the diagnostic performance of the penile brachial index and search for a specific cut-off point in this population. Accuracy was 69.3% (95% confidence interval: 58.6-78.7) for the detection of an arterial stenosis or occlusion on at least one side. The penile brachial index

Low-dose aspirin is largely but non-homogeneously used in primary prevention of cardiovascular complication in type-2 diabetic patients. We hypothesised that low-dose aspirin could interfere with the cutaneous neurovascular responses in type-2 diabetic patients. Galvanic current-induced vasodilatation (CIV) is an original non-noxious integrative model of neurovascular interaction and is impaired under low-dose aspirin in healthy subjects. Twenty type-2 diabetic patients (ten not receiving aspirin: D(-NA) and ten regularly receiving

Objectives: Endothelial dysfunction has been proposed as a potential mechanism implicated in the pathogenesis of cardiovascular complications of obstructive sleep apnea syndrome (OSAS). This study aimed to evaluate the microvascular endothelial function (MVEV) in OSAS and the impact on MVEF of 2 months of treatment with continuous positive airway pressure (CPAP) and mandibular advancement device (MAD)., Methods: Microvascular reactivity was assessed using laser Doppler flowmetry combined with acetylcholine (Ach) and sodium nitroprusside (SNP) iontophoresis in 24 OSAS patients and 9 control patients. In 12 of the 24 OSAS patients, microvascular reactivity was reassessed after 2 months of CPAP and MAD using a randomized cross-over design., Results: Ach-induced vasodilation was significantly lower in OSAS patients than in matched controls and correlated negatively with apnea hypopnea index (r=-0.49, p<0.025) and nocturnal oxygen desaturations (r=-0.63, p<0.002). Ach-induced vasodilation increased significantly with both CPAP and MAD. The increase in Ach-induced vasodilation under OSAS treatment correlated with the decrease in nocturnal oxygen desaturations (r=0.48, p=0.016)., Conclusion: Our study shows an impairment of MVEF in OSAS related to OSAS severity. Both CPAP and MAD treatments were associated with an improvement in MVEF that could contribute to improve cardiovascular outcome in OSAS patients.

The sense of touch is one of the most vital; still, it is incompletely understood. We review the afferent function that allows for the relay of sensory information from the periphery (the skin) to the central nervous system. Within this afferent function, we examine the different integrating levels including several candidates for cutaneous transducers, the conduction of the information via the afferent nervous fibres and the transmission of the sensory stimuli to higher brain structures, resulting in the perception of the different senses. We then examine the efferent system that stimulates the skin by secreting neurotransmitters. Finally, we discuss the tools available to study the cutaneous neurovascular interaction and conclude on a novel test that assesses this interaction triggered by the application of a local non noxious pressure (tactile stimulation).

Objective: To ascertain pressure ulcer prevalence rate in French hospitals., Method: In 2004, a cross-sectional study was conducted in all French hospitals, except university hospitals. The National Pressure Ulcer Advisory Panel (NPUAP) staging was used. Data were collected using two self-administered questionnaires., Results: A total of 37,307 inpatients in 1170 wards in 1149 hospitals were assessed, representing a response rate of 93.5%. Their mean age was 72.3 years and 62% were females. In all, 3314 patients had at least one pressure ulcer, giving a prevalence rate of 8.9%. A total of 4991 pressure ulcers were recorded; 64% of the patients had only one pressure ulcer. Fifty-five per cent of the patients had at least two concomitant diseases. When patients with only one ulcer were assessed, the most common locations were the heels (53%) and sacrum (29%). Heel pressure ulcers were more common in patients with obliterative arterial disease, and sacral pressure ulcers were more frequent in incontinent (urine, faecal and double incontinence) patients. Patients with multiple pressure ulcers had more severe lesions., Conclusion: These results indicate that the prevalence of pressure ulcers in French hospital inpatients has remained stable since the last prevalence study undertaken 10 years before, when the rate was 8.9%. Such studies should be encouraged in all health-care settings as a means of improving the care provided.

We previously showed a prolonged inhibition of current-induced vasodilation (CIV) after a single oral high dose of aspirin. In this study, we tested the hypothesis of platelet involvement in CIV. Nine healthy volunteers took 75 mg aspirin/day, 98 mg of clopidogrel bisulfate/day, or placebo for 4 days. CIV was induced by two consecutive 1-min anodal current applications (0.08 mA/cm(2)) through deionized water with a 10-min interval. CIV was measured with laser Doppler flowmetry and expressed as a percentage of baseline cutaneous vascular conductance: %C(b). In a second experiment in 10 volunteers, aspirin and placebo were given as in experiment 1, but a 26-h delay from the last aspirin intake elapsed before ACh iontophoresis and postocclusive hyperemia were studied in parallel to CIV. In experiment 1, the means +/- SE amplitude of CIV was 822 +/- 314, 313 +/- 144, and 746 +/- 397%C(b) with placebo, aspirin (P < 0.05 from placebo and clopidogrel), and clopidogrel (NS from placebo), respectively. In experiment 2, CIV impairment with aspirin was confirmed: CIV amplitudes were 300 +/- 99, and 916 +/- 528%C(b) under aspirin and placebo, respectively (P < 0.05), whereas vasodilation to ACh iontophoresis (322 +/- 74 and 365 +/- 104%C(b)) and peak postocclusive hyperemia (491 +/- 137 and 661 +/- 248%C(b)) were not different between aspirin and placebo, respectively. Low-dose aspirin, even 26 h after oral administration, impairs CIV, while ACh-mediated vasodilation and postocclusive hyperemia are preserved. If platelets are involved in the neurovascular mechanism triggered by galvanic current application in humans, it is likely to occur through the cyclooxygenase but not the ADP pathway.

Background: Little is known about the prevalence of proximal (hip, buttock, lower back) claudication after aortobifemoral bypass (AF2B) grafting and its hemodynamic effects at the buttock level., Methods: Forty-eight patients performed a treadmill test before and within 6 months after AF2B. The San Diego Claudication Questionnaire and the chest-corrected decrease from rest of transcutaneous oxygen pressure on buttocks were used to study exercise-induced proximal claudication and regional pelvic blood flow impairment. A decrease from rest of transcutaneous oxygen pressure value <-15 mm Hg was used to indicate regional blood flow impairment (RBFI)., Results: Patients had the following characteristics: 39 were men and 9 were women, 60 +/- 9 years, lowest ankle-to-brachial index (ABI) of 0.55 +/- 0.18 and maximal walking distance (MWD) on treadmill of 188 +/- 192 m at inclusion. ABI and MWD were significantly improved after surgery at 0.83 +/- 0.19 and 518 +/- 359 m (P < 0.0001). Unilateral or bilateral RBFI at the buttocks was found in 39 versus 29 patients before and after AF2B, respectively. Proximal claudication with underlying RBFI on one or both sides on treadmill were observed in 29 patients before AF2B, and in 9 of 26 (41%) versus 6 of 22 (23%) patients in end-to-end versus end-to-side proximal aorto-graft anastomosis of the AF2B, respectively (P < 0.05)., Conclusion: A significant increase in MWD and ABI, but little improvement of proximal perfusion is observed after surgery, a finding that is expected from the absence of hypogastric artery revascularization. The prevalence of proximal claudication and proximal blood flow impairment is higher in case of end-to-end when compared with end-to-side proximal aorto-graft anastomosis, confirming the role of collaterals such as lumbar arteries in the buttock circulation during exercise in patients suffering from peripheral arterial disease. Proximal claudication on treadmill early after surgery affects almost one third of the patients and must not be underestimated among patients receiving AF2B. Attempts at hypogastric artery revascularization, if possible, might be preferable to decrease the risk of proximal claudication after AF2B.

There is now strong evidence that an endothelium-derived hyperpolarizing factor (EDHF), other than nitric oxide (NO) or prostaglandin (PG), exists for dilating arteries and arterioles. In vitro studies on isolated vessels pointed out a role for EDHF as a back-up mechanism when the NO pathway is impaired, but there was a lack of in vivo studies showing a functional role for EDHF. Ageing has pronounced effects on vascular function and particularly on endothelium-dependent relaxation, providing a novel situation in which to assess the contributions of EDHF. The purpose of the present study was thus to determine if, in vivo, there was a functional role for EDHF as a back-up mechanism in the cutaneous microcirculation in the ageing process. We investigated in vivo the contribution of each endothelial factor (NO, PG and EDHF) in the cutaneous vasodilatation induced by iontophoretic delivery of acetylcholine and local pressure application in young adult (6-7 months) and old (22-25 months) mice, using pharmacological inhibitors. The cutaneous vasodilator responses induced by acetylcholine and local pressure application were dependent upon NO and PG pathways in young adult mice, whereas they were EDHF-dependent in old mice. EDHF appears to serve as a back-up mechanism when ageing reaches pathological states in terms of the ability for NO and PG to relax cutaneous microvessels, allowing for persistent cutaneous vasodilatator responses in old mice. However, as a back-up mechanism, EDHF did not completely restore cutaneous vasodilatation, since endothelial responses were reduced in old mice compared to young adult mice.

The TWIK related K+ channel TREK1 is an important member of the class of two-pore-domain K+ channels. It is a background K+ channel and is regulated by hormones, neurotransmitters, intracellular pH and mechanical stretch. This work shows that TREK1 is present both in mesenteric resistance arteries and in skin microvessels. It is particularly well expressed in endothelial cells. Deletion of TREK1 in mice leads to an important alteration in vasodilation of mesenteric arteries induced by acetylcholine and bradykinin. Iontophoretic delivery of acetylcholine and bradykinin in the skin of TREK1+/+ and TREK1-/- mice also shows the important role of TREK1 in cutaneous endothelium-dependent vasodilation. The vasodilator response to local pressure application is also markedly decreased in TREK1-/- mice, mimicking the decreased response to pressure observed in diabetes. Deletion of TREK1 is associated with a marked alteration in the efficacy of the G-protein-coupled receptor-associated cascade producing NO that leads to major endothelial dysfunction.

The aim of the study was to estimate the functional contribution of the arterial inflow pathways to the pelvic circulation during walking in patients with stage 2 lower extremity arterial disease. Transcutaneous oxygen pressure (Ptc(O(2))) changes during exercise can be used to estimate the severity of regional blood flow impairment while walking. Seventy patients with stable lower limb claudication were studied using a multivariate linear regression model. The relationship between exercise-induced buttock Ptc(O(2)) changes, the ipsilateral calf Ptc(O(2)) changes, and the arterial diameters of the pelvic arteriographic pathways were analyzed. The ipsilateral hypogastric and lumbar pathway, as well as the ipsilateral calf Ptc(O(2)) changes, were the only variables significantly related to buttock Ptc(O(2)) changes (r = 0.47; P < 0.001). Their normalized respective contribution to the regressive model was 39%, 19%, and 18%. None of the contralateral hypogastric, mesenteric, and sacral pathways or pathways stemming from the external iliac artery showed significant correlation to buttock Ptc(O(2)) changes. The ipsilateral hypogastric and ipsilateral lumbar pathways are the major pathways responsible for the functional buttock blood flow supply during walking. The role of contralateral hypogastric, inferior mesenteric, and median sacral pathways and arteries distal to the internal iliac trunk is negligible in the normal or compensatory blood flow supply. Distal Ptc(O(2)) decrease at exercise aggravates proximal Ptc(O(2)) decrease, possibly through the occurrence of a "steal phenomenon" of distal over proximal circulation during walking.

Pain is regarded as a risk factor in pressure ulcer development by contributing to immobility. Pressure-induced vasodilatation (PIV) is a mechanism whereby cutaneous blood flow increases in response to progressive locally applied pressure, thereby delaying the occurrence of ischaemia and appearing to be a protective response to local pressure. When the interaction between nervous and vascular systems is deregulated, PIV, which relies on both systems, is absent. We thus hypothesized that acute pain could alter PIV. This study investigated the effects on PIV of acute pain triggered by noxious heat (50 degrees C) applied to the tail of anaesthetized rats. To address the mechanisms underlying these effects, chronic sympathectomy was performed using guanethidine, and the plasma concentrations of pituitary adrenocorticotrophin (ACTH) and catecholamines were measured. Our results show that acute pain induces a loss of PIV associated with an increase of ACTH. Direct involvement of hypertensive effects and peripheral sympathetic nervous system are excluded in the loss of PIV, whereas the activation of brain structures that have descending inhibitory control cannot be excluded. A low dose of systemic morphine prevented this loss of PIV and maintained the ability of the cutaneous microcirculation to adapt to the applied pressure. The loss of a protective response to local pressure (PIV) induced by acute pain lends physiological support to the direct involvement of pain in pressure ulcer development. Therefore, an adequate evaluation and treatment of pain is crucial.

Background: Proximal (ie, buttock, hip) claudication can result from impaired perfusion in the hypogastric area after aortobifemoral bypass (ABF) despite normal femorodistal blood flow provided by the patent bypass. The proportion of patients that experience proximal claudication after ABF is unknown, and arguments for the vascular origin of symptoms specifically at the proximal level have never been reported., Methods: This was a prospective study set in an institutional practice of ambulatory patients referred for a systematic survey of their previous ABF bypass. Among the 131 eligible patients, 10 refused to participate and 16 were unable to walk on a treadmill. The 105 studied patients (94 men, 11 women) were a mean age of 63 +/- 10 years, and the median delay from surgery was 2 years (range, 4 months to 26 years). We used a modified version of the San Diego Claudication Questionnaire administered both at rest before the treadmill study and again after the treadmill test. Transcutaneous oxygen pressure (TcPO2) at the buttock level was used to evaluate blood flow impairment during exercise at the proximal level, with blood flow impairment defined as buttock minus chest TcPO2 decrease in excess of -15 mm Hg., Results: Thirty patients reported proximal exercise-related pain consistent with vascular criteria by history before exercise. However, 59 patients (56%) reported symptoms compatible with proximal claudication, and TcPO2 values were abnormal on one or both sides in 52. The persistence of at least one (prograde or retrograde) pathway to the hypogastric circulation, determined by review of operative details from the aortobifemoral bypass and angiography, did not significantly decrease the proportion of patients reporting proximal claudication by history (26%) or on treadmill (55%) compared with those with bilateral hypogastric occlusion (33% by history, P = .51 compared with at least one prograde hypogastric pathway and 61% based on treadmill test, P = .65 compared with at least one prograde hypogastric pathway)., Conclusion: The present study shows that (1) the proportion of ABF patients with a median bypass age of 2 years that report proximal claudication is high (28%), (2) this proportion is significantly higher when claudication is detected by treadmill exercise tests, (3) a vascular origin (or at least contribution) is likely 88% of the proximal symptoms observed on treadmill, (4) the presence of proximal claudication with associated abnormal TcPO(2) results increases the risk of walking impairment in affected patients, and (5) preservation of at least one internal iliac artery to allow prograde or retrograde flow to the hypogastric vascular bed does not decrease the risk of proximal claudication after ABF surgery. A vascular origin of (or at least contribution to) most of the proximal exercise-related symptoms should always be discussed in patients with patent ABF bypass.

Aim: Measurement of transcutaneous oxygen pressure (tcpO2) is of interest in critical limb ischemia at rest and also during exercise in patients suffering proximal claudication or claudication of questionable origin. The recent commercialization of the computerized multiprobe-TCM400 device (Radiometer, Copenhagen, DK) appears attractive for exercise tests but comparison with the previous devices has not been reported. Indeed, the final endpoint for the physician is to be sure that a new apparatus will not interfere with the results observed in patients., Methods: Using a 5 probe-TCM400 and 5 single probe-TCM3s, simultaneous recordings of tcpO2 were performed: 1) in vitro during 25 simulated exercises and 2) in vivo during exercise treadmill tests in 27 vascular patients. We analyzed resting (REST), minimal absolute (MIN) and DROP (limb-changes minus chest-changes) values. TcpO2 absolute and DROP profiles were analyzed through cross-correlation to detect response delays between the devices., Results: In simulated tests, the Pearson coefficient of correlation between TCM400 and TCM3 was r=0.99 for REST, MIN and minimal DROP. In treadmill tests, the Pearson coefficient of correlation between TCM400 and TCM3 was significantly higher with minimal DROP (r=0.88) than with REST (r=0.63) or MIN (r=0.7). A 15 s delay was observed with TCM3 as compared to TCM400 responses for both tcpO2 and DROP profiles. The rmax(2) of the cross-correlation was 0.74 and 0.67 for tcpO2 and DROP, respectively., Conclusions: Our observations underline the limits of the clinical in vivo comparison of 2 transcutaneous devices. Despite the differences observed in absolute values during in vivo tests with simultaneous recordings (assumed to rely on physiological and not technical problems), we suggest that TCM400 is valid for exercise tests with the advantage of improved user interface, automatic memorization and integrated multiple probes of this newly commercially available apparatus.

Pressure-induced vasodilation, a neurovascular mechanism relying on the interaction between mechanosensitive C-fibers and vessels, allows skin blood flow to increase in response to locally nonnociceptive applied pressure that in turn may protect against pressure ulcers. We expected that severe neuropathy would dramatically affect pressure-induced vasodilation in diabetic mice, and we aimed to determine whether pressure-induced vasodilation alteration could be reversed in 8-week diabetic mice. Control and diabetic mice received no treatment or sorbinil, an aldose reductase inhibitor, or alagebrium, an advanced glycation end product breaker, the last 2 weeks of diabetes. Laser Doppler flowmetry was used to evaluate pressure-induced vasodilation and endothelium-dependent vasodilation after iontophoretic delivery of acetylcholine (ACh). We assessed the nervous function with measurements of motor nerve conduction velocity (MNCV) as well as the C-fiber-mediated nociception threshold. Pressure-induced vasodilation, endothelial response, C-fiber threshold, and MNCV were all altered in 8-week diabetic mice. None of the treatments had a significant effect on MNCV. Although sorbinil and alagebrium both restored ACh-dependent vasodilation, sorbinil was the sole treatment to restore the C-fiber threshold as well as pressure-induced vasodilation development. Therefore, the inhibition of aldose reductase pathway by sorbinil improved vascular and C-fiber functions that allow pressure-induced vasodilation restoration that could limit neuropathic diabetic cutaneous pressure ulcers.

The development of sports activities in the over forties has increased the number of middle-aged patients performing heavy-load exercise. The normal response of ankle systolic blood pressure (ASBP) and ankle to brachial index (ABI) to intense exercise is known in young athletes, but little is known for other age groups. Three groups of 21 athletes: <20 (G1), 20-40 (G2), and >40 (G3) years old, respectively, were studied. ASBP and brachial systolic blood pressure (BSBP) were measured simultaneously before and after an incremental maximal cycle ergometer test. Rest ABI was higher in G3 compared to G1 (P<0.001: ANOVA, Bonferroni). Compared to respective resting values, BSBP, at 1 min of recovery, was increased for the three groups of age (P<0.001) whereas ASBP was unchanged for G1 and G2, and significantly increased for G3 (P<0.001). ASBP was significantly higher in G3 than in G1 and G2, ABI was lower in G1 and G2 compared to G3: 0.70+/-0.11, 0.76+/-0.09 and 0.91+/-0.14, respectively. This age-related ABI increase is consistent with the impaired vasodilator capacity observed in aging normal subjects but not with the decrease observed in ABI resting values in epidemiological studies. ABI is higher in older than in younger athletes at rest and after exercise. In aging athletes, aiming to detect mild to moderate arterial lesions, it is likely that normal limits defined in young athletes are not valid.

Objective: Pressure-induced vasodilation (PIV) allows skin blood flow to increase in response to locally applied pressure and may be protective against pressure ulcers. We previously showed that PIV was absent in 1-week diabetic mice exhibiting no neuropathy. Our aim was to determine whether the diabetes-induced PIV alteration could be prevented., Methods and Results: Diabetic mice received no treatment or a daily treatment with either sorbinil, alagebrium or alpha-lipoic acid (LPA) for 1 week. Laser Doppler flowmetry was used to evaluate PIV as well as endothelium-dependent vasodilation following iontophoretic delivery of acetylcholine (ACh). The effect of each treatment on oxidative stress was examined by plasma 8-isoprostane assay. LPA was the sole treatment to prevent both PIV and ACh vasodilation alterations, with a significant reduction of oxidative stress in diabetic mice. Both PIV and ACh-vasodilation were abolished in LPA-treated diabetic mice following injection of Nomega-nitro-L-arginine (p<0.05). In contrast, alagebrium and sorbinil prevented neither diabetes-induced PIV abolition nor endothelial alteration., Conclusions: LPA treatment significantly reduced the oxidative stress and was able to preserve endothelial nitric oxide availability in the cutaneous microcirculation and then to preserve the PIV response in diabetic mice. LPA treatment could play a key role in limiting the risk of pressure-induced cutaneous ulcer during diabetes.

Background: Very few observations of proximal-without-distal claudication have been reported in the literature. This is likely due to the use of questionnaires limiting vascular claudication to the calves and to the problems encountered in attributing unexplained "buttock" claudication to a vascular origin., Methods: During a 2 1/2-year period, we searched for proximal-without-distal exercise-related pain with the San Diego claudication questionnaire among some 2000 patients referred for lower limb arterial investigations. Of these patients, 97 presented no contraindication to treadmill testing and were investigated with exercise transcutaneous oxygen pressure (tcpO2). We used buttock tcpO2 (DROP index<-15 mm hg) to argue for the presence of ischemia on the corresponding side., Results: Ischemia consistent with symptoms was found in 61 patients, whereas pain on one or both sides without underlying ischemia was found in 36 patients, suggesting a non-arterial origin of the symptoms. More than half of the patients with proximal-without-distal claudication and underlying exercise-related ischemia had been suffering for more than 2 years before they were referred to the laboratory. Eleven of the patients were treated. The treatment was successful in all but one of them., Conclusions: An important delay before diagnosis is frequently observed in proximal-without-distal claudication. TcpO2 is useful in attributing proximal exercise-related pain to a vascular origin. Given the number of detected and successfully treated patients in this small monocentric study, it is surprising that so few observations have been published to date, suggesting that proximal-without-distal arterial claudication is most likely an underestimated diagnosis.

Assumed to rely on an axon reflex, the current-induced vasodilation (CIV) interferes with the microvascular response to iontophoretic drug delivery. Mechanisms resulting in CIV are likely different at the anode and at the cathode. While studies have been conducted to understand anodal CIV, little information is available on cathodal CIV. The present study investigates CIV observed following 0.1-mA cathodal applications on forearms of healthy volunteers and the possible mechanisms involved. Results are expressed in percentage of the cutaneous heat-induced maximal vascular conductance [%MVC (means +/- SE)]. 1) The amplitude of CIV was proportional to the duration of cathodal currents for periods of <1 min: r = 0.99. 2) Two current applications of 10 s, with 10-min interstimulation interval, induced a higher peak value of CIV (79.1 +/- 8.6% MVC) than the one obtained with all-at-once 20-s current application (39.5 +/- 4.3% MVC, P < 0.05). This amplified vascular response due to segmental application was observed for all tested interstimulation intervals (up to 40 min). 3) Two hours and 3 days following pretreatment with 1-g oral aspirin, the CIV observed following cathodal application, as well as the difference of cathodal CIV amplitude between all-at-once and segmented applications, were reduced. These findings suggest a role of prostaglandins, not only released from endothelial or smooth muscle cells, as direct vasodilator and/or as a sensitizer. Thus aspirin pretreatment could be used to decrease CIV resulting from all-at-once and repeated cathodal application and facilitate the study of the specific vascular effect induced by the drug delivered.

In the skin of humans and rodents, local pressure induces localized cutaneous vasodilation, which may be protective against pressure-induced microvascular dysfunction and lesion formation. Once activated by the local pressure application, capsaicin-sensitive nerve fibers release neuropeptides that act on the endothelium to synthesize and release nitric oxide (NO) and prostaglandins, leading to the development of the cutaneous pressure-induced vasodilation (PIV). The present study was undertaken to test in vivo the hypothesis that PIV is mediated or modulated by differential activation of K+ channels in anesthetized rats using pharmacological methods. Local pressure was applied at 11.1 Pa/s. Endothelium-independent and -dependent vasodilation were tested using iontophoretic delivery of sodium nitroprusside (SNP) and acetylcholine (ACh), respectively, and was correlated with PIV response. PIV was reduced after systemic administration of tetraethylammonium (a nonspecific K+ channel blocker), iberiotoxin [a specific large-conductance Ca2+-activated K+ (BKCa) channel blocker], and glibenclamide [a specific ATP-sensitive K+ (KATP) channel blocker], whereas PIV was unchanged by apamin (a specific small-conductance Ca2+-activated K+ channel blocker) and 4-aminopyridine (a specific voltage-sensitive K+ channel blocker). The responses to SNP and ACh were reduced by iberiotoxin but were unchanged by glibenclamide. We conclude that the cellular mechanism of PIV in skin involves BKCa and KATP channels. We suggest that the opening of BKCa and KATP channels contributes to the hyperpolarization of vascular smooth muscle cells to produce PIV development mainly via the NO and prostaglandin pathways, respectively.

Background: Noninvasive tests are required to detect (in both male and female subjects and side by side) arteries toward the hypogastric circulation that are likely to present significant lesions as a cause of buttock claudication., Methods: We compared the accuracy of near-infrared spectroscopy (NIRS) and transcutaneous oxygen pressure (TCP o 2 ) on both buttocks during walking tests to detect lesions on the arteries toward the hypogastric circulation. NIRS was considered abnormal if recovery time to pre-exercise values was greater than 240 seconds for tissue oxygen saturation (absent data being coded 0), and TCP o 2 was coded abnormal if the minimal value of buttock changes minus chest changes was lower than -15 mm Hg. The study was conducted in a university hospital; there were 30 ambulatory patients with stage 2 claudication of the Fontaine classification., Results: Angiography showed 36 abnormal (stenosis > 75%) and 24 normal arterial axes toward the buttocks circulation. NIRS and TCP o 2 provided respectively 55% (range, 41.6% to 67.9%) and 82% (range, 69.6% to 90.5%) accuracy (95% confidence interval) to predict the presence of arteriographically proven lesions; P < .05., Conclusions: Using available cut-off points proposed in the literature, NIRS showed a lower diagnostic accuracy than TCP o 2 for the prediction of lesions on the arterial tree to the hypogastric circulation. NIRS is a recent technique as compared with TCP o 2 , and its diagnostic accuracy might improve in the future. Currently, one should carefully weigh the advantages and limits of NIRS and TCP o 2 when a choice is to be made between them to monitor exercise-induced changes resulting from lower limb arterial disease at the proximal level.

It is generally acknowledged that cutaneous vasodilatation in response to monopolar galvanic current application would result from an axon reflex in primary afferent fibers and the neurogenic inflammation resulting from neuropeptide release. Previous studies suggested participation of prostaglandin (PG) in anodal current-induced cutaneous vasodilatation. Thus the inducible cyclooxygenase (COX) isoform (COX-2), assumed to play a key role in inflammation, should be involved in the synthesis of the PG that is released. Skin blood flow (SkBF) variations induced by 5 min of 0.1-mA monopolar anodal current application were evaluated with laser-Doppler flowmetry on the forearm of healthy volunteers treated with indomethacin (COX-1 and COX-2 inhibitor), celecoxib (COX-2 inhibitor), or placebo. SkBF was indexed as cutaneous vascular conductance (CVC), expressed as percentage of heat-induced maximal CVC (%MVC). Urinalyses were performed to test celecoxib treatment efficiency. No difference was found in CVC values at rest: 14.3 +/- 4.0, 11.9 +/- 3.2, and 10.9 +/- 2.0% MVC after indomethacin, celecoxib, and placebo treatment, respectively. At 10 min after the onset of anodal current application, CVC values were 22.2 +/- 4.9% MVC (not significantly different from rest) with indomethacin, 85.7 +/- 15.3% MVC (P < 0.001 vs. rest) with celecoxib, and 70.4 +/- 13.1% MVC (P < 0.001 vs. rest) with placebo. Celecoxib significantly depressed the urinary prostacyclin metabolite 6-keto-PGF(1alpha) (P < 0.05 vs. placebo). Indomethacin, but not celecoxib, significantly inhibited the anodal current-induced vasodilatation. Thus, although they are assumed to result from an axon reflex in primary afferent fibers and neurogenic inflammation, these results suggest that the early anodal current-induced vasodilatation is mainly dependent on COX-1-induced PG synthesis.

Aim: Although a time consuming technique, tcpO2 provides complementary information as compared to other tests. Simultaneous recording of systemic and peripheral oxygen pressure changes with exercise could be interesting to confirm that local hypoxemia is of arterial origin, but accuracy versus gold standard arteriography and objectively determined cut-off points to be used in arterial claudication at the ankle are not reported., Experimental Design: retrospective plus prospective study., Setting: institutional practice, ambulatory care., Patients: 100 patients suffering stage 2 claudication (group A) were retrospectively studied to objectively define cut-off points derived from tcpO2 recordings to be used in exercise testing. Then, applicability and reproducibility of these cut-off points were analysed prospectively in another 50 patients (group B)., Intervention: tcpO2 was measured on both calves and with a chest reference electrode. Arteriography on each side was quoted positive for a diameter stenosis superior to 75% or occlusion on the aorto-popliteal axis or of all-3-calf arteries., Results: The best performance was obtained with tcpO2 changes from rest at the calf normalised to eventual chest changes (DROP) during or following the treadmill test. Optimal cut-off point determined through ROC curve analysis for DROP was -15 mmHg in group A. Applying this cut-off point in group B provided a 86/84% sensitivity/specificity and showed excellent reproducibility., Conclusions: TcpO2 measurement on the calf during exercise could be useful in a selected population of patients with claudication of questionable vascular origin and/or when other non-invasive investigations cannot be performed.

Prolonged external pressure can cause pressure sores. We examined the link between mechanical sensitivity and cutaneous vasodilation, and its possible alteration in patients at high risk of pressure sores. Clinical and experimental studies have shown that this link, which is not dependent on inflammation or pain, involves capsaicin-sensitive nerve fibers. Receptors for calcitonin gene-related peptide, vasoactive intestinal peptide and pituitary adenylate cyclase-activating polypeptide are also involved, contrary to neurokinin receptors. Endothelial nitric oxide is crucialfor pressure-induced vasodilation. This link is altered in diabetes, even prior to the onset of nervous complications. Restoration of pressure-induced vasodilation might prevent the onset of pressure sores and plantar ulcers in diabetic patients.

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 (CVC(20)). 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; CVC(20): 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 CVC(20) 29 +/- 6%MVC. At day 3, CVC(peak) was 53 +/- 9, CVC(min) 22 +/- 3 and CVC(20) 25 +/- 4%MVC. At day 10, CVC(peak) was 67 +/- 10, CVC(min) 47 +/- 7 and CVC(20) 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.

Among the last 250 claudicants referred to the laboratory for transcutaneous oxygen pressure recording at exercise, we analyzed the symptoms reported by the 36 patients who showed isolated proximal (without distal) ischemia. Among the symptomatic proximal sites cited by these patients, the hip and thigh represent 60%, whereas the buttock is cited in fewer than 25% of cases. Buttock symptoms are reported in only 31% of symptomatic patients. 'Buttock' claudication is probably not the dominant symptom in isolated proximal vascular ischemia. Assessing proximal lower limb ischemia through the sole detection of 'buttock pain' could contribute to the underestimation of proximal vascular ischemia.

A significant transient increase in laser Doppler flowmetry (LDF) signals is observed in response to a local and progressive cutaneous pressure application in healthy subjects. This reflex may be impaired in diabetic patients. The work presents a signal processing providing the clarification of this phenomenon. Scalogram analyses of LDF signals recorded at rest and during a local and progressive cutaneous pressure application are performed on healthy and type 1 diabetic subjects. Three frequency bands, corresponding to myogenic, neurogenic and endothelial related metabolic activities, are studied. The results show that, at rest, the scalogram energy of each frequency band is significantly lower for diabetic patients than for healthy subjects, but the scalogram relative energies do not show any statistical difference between the two groups. Moreover, the neurogenic and endothelial related metabolic activities are significantly higher during the progressive pressure than at rest, in healthy and diabetic subjects. However, the relative contribution of the endothelial related metabolic activity is significantly higher during the progressive pressure than at rest, in the interval 200-400 s following the beginning of the pressure application, but only for healthy subjects. These results may improve knowledge on cutaneous microvascular responses to injuries or local pressures initiating diabetic complications.

Due to their small size, lipid nanocapsules (LNC) might be promising for an injectable as well as for an oral drug delivery system, providing both sufficient drug solubility avoiding vessel embolisation for the intravenous injection and a positive effect of drug absorption after oral administration. Biocompatible ibuprofen LNC were developed in a size range of around 50 nm with a new preparation method. Drug incorporation into LNC was successful to a high degree in all formulations tested (94-98%) and the in vitro drug release in phosphate buffer occurred within 24 h. Pharmacokinetic data were recorded in vivo from rats after intravenous or oral administration, while the antinociceptive efficiency of the LNC formulation was compared with ibuprofen solution by the tail flick test. The AUC and half-life of intravenously injected ibuprofen LNC were found to be 16 and 19%, respectively, higher than a simple drug solution, while the mean residence time was not changed. Oral administration of LNC showed an 18% increase of AUC and a 27% higher mean residence time. The antinociceptive effect was similar for oral administration, drug solution, and LNC at 30 min after administration, and was prolonged up to 4 h in the LNC group. The pain relief after intravenous administration was prolonged when administering LNC formulation for at least 2 h. A drug delivery system for intravenous administration of ibuprofen has been developed which exhibits sustained release properties by either oral or intravenous route and may be interesting in the treatment of postoperative pain.

Pressure-induced vasodilation (PIV) is a mechanism whereby skin blood flow increases in response to progressive locally applied pressure. Skin blood flow in response to applied pressure decreased early in diabetic patients as a result of vascular and/or neural impairment. This study was designed to determine the effect of vascular changes on PIV in 1-week streptozotocin-induced diabetic mice. We assessed cutaneous microvascular response to local increasing pressure application measured by laser Doppler flowmetry (LDF) and endothelium-dependent and -independent vasodilation by iontophoretic delivery of acetylcholine and sodium nitroprusside and sciatic motor nerve conduction velocity and morphometry. In control mice, LDF increased 34% from baseline to 0.2 kPa external pressure, showing PIV response. In contrast, diabetic mice had no LDF increase in response to progressive external pressure. Moreover, after iontophoretic delivery of acetylcholine, endothelium-dependent vasodilation was largely attenuated in diabetic mice (25%) compared with control mice (81%), whereas vasodilation to sodium nitroprusside was not different between groups. Nerve function as assessed by sciatic nerve conduction velocity and morphometry did not differ between groups. These findings suggest that endothelial impairment is sufficient to severely alter PIV response, which seems to be highly sensitive to endothelial nitric oxide levels. PIV suppression could favor diabetes complications such as diabetic foot ulcers.

Aim: Although transcutaneous oxygen pressure measurements (tcpO2) are largely used in the investigation of vascular patients, its reproducibility is still debated. Indeed an unpredictable gradient exists between arterial and transcutaneous oxygen pressure. We hypothesised that indices taking into account changes over time and independent of absolute starting values would be more reproducible than other indices., Experimental Design: comparative test-retest procedure (1 to 13 days between tests)., Settings: institutional practice, ambulatory care., Patients and Participants: 15 subjects with stage 2 claudication., Interventions: tcpO2 recordings at rest and at exercise during the 2 treadmill tests., Measures: calculation of the Delta-from-rest of oxygen pressure index (limb tcpO2 changes minus chest tcpO2 changes), of the resting - or minimal values attained during exercise - of absolute tcpO2 and of the regional perfusion index (regional perfusion index: ration of limb to chest)., Results: Both absolute tcpO2 and regional perfusion index at rest showed low reproducibility. During exercise the best reproducibility was attained through Delta-from-rest of oxygen pressure index calculation. Equations from the linear regression analysis (test 2 versus test 1) were 0.88 x -4.2 (r(2)=0.82) at the buttock level and 0.82 x -3.8 (r(2)=0.80) at the calf level., Conclusion: TcpO2 measurement on the calf or buttock during exercise, is a reproducible measurement in patients with vascular claudication, specifically when corrected for exercise-induced systemic pO2 changes trough Delta-from-rest of oxygen pressure calculation.