Chest tcpO2 changes during constant-load treadmill walking tests in patients with claudication.

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.

Cutaneous neurovascular interaction involved in tactile sensation.

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).

A national prevalence study of pressure ulcers in French hospital inpatients.

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.

Platelet inhibition by low-dose aspirin but not by clopidogrel reduces the axon-reflex current-induced vasodilation in humans.

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.

Validation of a new device for transcutaneous oxygen pressure recordings in real and simulated exercise tests.

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.

Systematic diagnostic approach to proximal-without-distal claudication in a vascular population.

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.

Cathodal current-induced vasodilation to single application and the amplified response to repeated application in humans rely on aspirin-sensitive mechanisms.

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.

Transcutaneous oxygen pressure measurements (tcpO2) at ankle during exercise in arterial claudication.

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.

Prostaglandins participate in the late phase of the vascular response to acetylcholine iontophoresis in humans.

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.

Reproducibility of proximal and distal transcutaneous oxygen pressure measurements during exercise in stage 2 arterial claudication.

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.

Anodal current intensities above 40 microA interfere with current-induced axon-reflex vasodilatation in human skin.

When using iontophoresis, the 'non-specific' vasodilatation (NSV) that is observed as a result of C-fibre excitation is generally attributed to the local accumulation of protons under the anode. NSV following prolonged 100-microA anodal current application only appears after the current is stopped. Break excitation alone does not explain the delayed onset of this vasodilatation. We hypothesised that this delay could result from an anodal block and thus, that a minimal intensity would be required to achieve hyperpolarisation of primary afferent fibres (mainly C-fibres). Using laser Doppler flowmetry, cutaneous blood flow was recorded in the forearms of 8 healthy volunteers 2 min before current application, during the application and 20 min after stopping the monopolar anodal current. In protocol 1, after 2.5 min of current application at an intensity of 100 microA, the intensity was abruptly decreased to 0-80 microA for a second 2.5-min period. The onset of vasodilatation was only delayed at intensities >30 microA during this second period. In protocol 2, re-application of the current after a 50-second interruption (expected to allow for the occurrence of an axon reflex) did not interfere with the onset of vasodilatation. Thus: (1) the minimal intensity interfering with the axon reflex is far lower than that reported for C-fibre blockade in isolated nerves; (2) the results suggest that current application does not directly interfere with the vasodilator mechanisms induced by the axon reflex at the level of smooth muscle cells.

Prolonged aspirin inhibition of anodal vasodilation is not due to the trafficking delay of neural mediators.

We previously reported that forearm vasodilation to a delivered all-at-once over 5 min or a 1-min repeated monopolar anodal 0.10-mA current application is aspirin sensitive and that a single high-dose aspirin exerts a long-lived effect in the former case. We hypothesized that 1) in the latter case, the effect of aspirin would also be long lived and 2) the time required to resupply nerve endings with unblocked cyclooxygenase through axonal transport could explain this phenomenon. We studied the time course for the recovery of vasodilation to repeated current application after placebo or 1-g aspirin treatment. We then searched for a difference at a proximal vs. distal site in the recovery of the response. Aspirin abolished current-induced vasodilation at 2 h, 10 h, and 3 days, with a progressive recovery thereafter, but no difference between distal and proximal site was observed for the recovery of the response. This suggests that, although neural cyclooxygenase could participate in the response, the time course of aspirin inhibition of current-induced cutaneous vasodilation is not due to the time required through neural transport to resupply nerve endings with unblocked proteins.

Oral single high-dose aspirin results in a long-lived inhibition of anodal current-induced vasodilatation.

1 Acetyl salicyclic acid (aspirin) irreversibly blocks cyclo-oxygenase (COX). This effect is short-lived in endothelial or smooth muscle cells due to resynthesis but long-lived in platelets devoid of synthesis ability. Aspirin blocks the anodal current-induced vasodilatation, suggesting participation by prostaglandin (PG). We analysed the time course of the effect of aspirin as an indirect indicator of the origin of the PG possibly involved in anodal current-induced vasodilatation. 2 In healthy volunteers, vasodilatation, estimated from the peak cutaneous vascular conductance (CVC(peak)), was recorded in the forearm during and in the 20 min following 5 min, 0.10 mA transcutaneous anodal current application, using deionized water as a vehicle. CVC(peak) was normalized to 44 degrees C heat-induced maximal vasodilatation and expressed in per cent values. Experiments were performed before and at 2 and 10 h, 3, 7, 10 and 14 days after blinded 1-g aspirin or placebo treatment. 3 CVC(peak) (mean+/-s.d.mean) after aspirin vs placebo was 13.6+/-14.5 vs 65.0+/-32.1 (P<0.05) 14.7+/-4.2 vs 87.5+/-31.9 (P<0.05), 18.1+/-10.2 vs 71.6+/-26.8 (P<0.05), 42.5+/-23.4 vs 73.3+/-26.8 (non significant, NS), 60.2+/-24.3 vs 75.2+/-26.9 (NS), 52.1+/-18.5 vs 67.9+/-32.1 (NS) at 2 and 10 h and at days 3, 7, 10 and 14 respectively. 4 Aspirin inhibition of anodal current-induced vasodilatation persists long after endothelial and smooth muscle cyclo-oxygenases are assumed to be restored. This suggests that the PG involved in this response are not endothelial- or smooth muscle-derived. The underlying mechanism of this unexpected long-lived inhibition of vasodilatation by single high dose aspirin remains to be studied.

Break excitation alone does not explain the delay and amplitude of anodal current-induced vasodilatation in human skin.

In iontophoresis experiments, a 'non-specific' current-induced vasodilatation interferes with the effects of the diffused drugs. This current-induced vasodilatation is assumed to rely on an axon reflex due to excitation of cutaneous nociceptors and is weaker and delayed at the anode as compared to the cathode. We analysed whether these anodal specificities could result from a break excitation of nociceptors. Break excitation is the generation of action potentials at the end of a square anodal DC current application, which are generally weaker than those observed at the onset of a same application at the cathode. In eight healthy volunteers, we studied forearm cutaneous laser Doppler flow (LDF) responses to: (1) anodal and cathodal 100 microA current applications of 1, 2, 3, 4 or 5 min; (2) 100 microA anodal applications of 3 min with a progressive ending over 100 s (total charge 23 mC); these were compared to square-ended 100 microA anodal applications of the same total charge (23 mC) or duration (3 min); (3) a 4 min 100 microA anodal application with a 333 msec break at half time. Results (mean +/- S.D.) are expressed as percentage of heat-induced maximal vasodilatation (%MVD). Onset (T(vd)) and amplitude (LDF(peak)) of vasodilatation were determined. We observed that: T(vd) was linearly related to the duration of current application at the anode (slope = 1.01, r(2) = 0.99, P < 0.0001) but not at the cathode (slope = 0.03, r(2) = 0.02, n.s.). Progressive ending of anodal current did not decrease LDF(peak) (63.3 +/- 24.6 %MVD) as compared to square-ending of current application of the same duration (36.9 +/- 22.2 %MVD) or the same total charge (57.1 +/- 23.5 %MVD). A transient break of anodal current did not allow for the vasodilatation to develop until current was permanently stopped. We conclude that, during iontophoresis, anodal break excitation alone cannot account for the delay and amplitude of the vascular response.

Vasodilatation in response to repeated anodal current application in the human skin relies on aspirin-sensitive mechanisms.

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.

Spectral and profile analysis of Doppler recording following below-knee arterial distal bypasses.

BACKGROUND: Arterial below knee distal bypasses are associated with a high risk of thrombosis as compared to proximal bypasses. We assumed that before the bypass occludes, in the early postsurgical period, measurable velocity changes, and/or the presence of high intensity transient signals (HITS) would occur. SETTINGS: institutional reference center, hospitalized patients. SUBJECTS: satisfactory Doppler recording was obtained in 51 among 61 consecutive patients (32 males, 19 females, height: 165+/-7 cm, weight: 68+/-12 kg) suffering lower extremity arterial disease, that underwent saphenous (n=33), prosthetic (n=4) or sequential (n=14) below knee bypasses. We performed a spectral and profile analysis of a single postsurgical 2 hour Doppler recording at the ankle level and analyzed Doppler derived indices and clinical risk factors in the evaluation of the risk of bypass occlusion within 7 days following surgery. RESULTS: Primary patency at day 7 was observed in 41 of the 51 operated patients. The presence of HITS was found in approximately 30% of the patients and provided no information on the risk of thrombosis. No clinical variable was significantly associated with an increased risk of thrombosis. Whatever the duration of recording, the presence of a diastolic forward flow and wide systolic velocity changes were poor indicators of bypass thrombosis risk. On 512 beat recordings, a mean systolic velocity below 1630 Hz and a standard deviation of the resistance index >0.095 were associated with a 6.74 [1.6-28.4] (p<0.01) and 14.5 [3.6-58.9] (p<0.001) times increases in the risk of bypass occlusion respectively, compared with subjects that do not fulfill each criteria. CONCLUSIONS: Periods of transient asymptomatic no-flow-reflow events may be observed before the bypass irreversibly occludes. Prolonged Doppler recording should be preferred to short term analyses, to allow for the detection of these transient events and may provide potential indices for future research.

Current-induced vasodilation during water iontophoresis (5 min, 0.10 mA) is delayed from current onset and involves aspirin sensitive mechanisms.

Study of the microcirculation by iontophoresis is potentially confounded by any non-specific effects of current application. Laser Doppler flow (LDF, mean +/- SD; arbitrary units; AU) was recorded on the forearms of healthy volunteers during and 20 min following application of 0.10-mA current for 1, 3 and 5 min, using deionised water as a vehicle. Local heating to 44 degrees C was then applied for 24 min to assess maximal vasodilation. Cathodal current applications resulted in delayed and prolonged vasodilation (peak values: 78 +/- 29, 75 +/- 19, 80 +/- 37 AU) whereas anodal peak LDF was 13 +/- 6, 27 +/- 34 and 72 +/- 40 AU for 1-, 3- and 5-min periods of current applications, respectively. From current onset, inflexion points in the responses to 3- and 5-min anodal current applications occurred at 4.5 and 6.5 min, respectively, and at approximately 1.5 min for all cathodal current applications. For 5-min current applications: a preliminary tourniquet ischaemia neither changed the time course nor the amplitude of the response to current application. In this situation, local anaesthesia abolished the current-induced vasodilation. Chronic capsaicin pretreatment decreased the amplitude of the vasodilation. Pretreatment with 500 mg oral aspirin decreased the cathodal vasodilation and abolished the anodal vasodilation, even in the absence of preliminary ischaemia. We conclude that vasodilation to prolonged application of 0.10-mA continuous monopolar current after transient tourniquet ischaemia cannot be exclusively the result of an axon reflex initiated by current onset. This current-induced vasodilation is at least partly dependent on capsaicin-sensitive afferent fibres and relies on aspirin-sensitive mechanisms at both polarities.

Infra-stellate upper thoracic sympathectomy results in a relative bradycardia during exercise, irrespective of the operated side.

OBJECTIVE: Removal of accessory fibres coming from the sub-stellar thoracic chain to the heart during infra-stellate surgical upper thoracic sympathectomy (ISS) may be responsible for a decreased heart rate to workload relationship during exercise following surgery. We hypothesised that heart rate would decrease not only following right ISS. METHODS: We performed repeated bicycle incremental exercise tests in 11 control subjects (26.9+/-9.5 years, 61.4+/-12.4 kg, 167+/-10 cm), and 11 patients (29.8+/-10 years, 59.3+/-12.0 kg, 168+/-7 cm) referred for bilateral ISS: results are mean+/-standard deviation. Surgery was performed at two distinct times allowing to study the consequences of unilateral and bilateral sympathectomy to confirm whether a significant relative bradycardia was constant and dependent on the operated side. RESULTS: For control subjects, test durations were 13.55+/-3.29, 14.09+/-4.01 and 13.00+/-3.26 min and heart rates were 187+/-7, 187+/-8 and 186+/-7 beats min(-1) at the first, second and third test, respectively. Although time to exhaustion was comparable to controls and unchanged between tests: 12.32+/-2.87, 12.3+/-2.90, 12.33+/-3.76 min, heart rate at maximum exercise decreased significantly from 176+/-16 to 164+/-15, and 148+/-15 beats min(-1), before, following unilateral and bilateral ISS, respectively. The operated side did not allow for the prediction of the effect of unilateral sympathectomy. CONCLUSIONS: Patients should be informed of the exercise bradycardia resulting from ISS, although clinical tolerance seems excellent in endurance exercise. Contrary to previous reports at rest, during exercise no right-sided dominance was observed. These findings are consistent with reports of random distribution of sub-stellate cardiac fibres from anatomical studies.