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Biomedical subjects

J L Saumet

Publications and source records attributed to J L Saumet.

At least 19 recordsLinked to original sources
PubMed2006

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.

Blood Gas Monitoring, Transcutaneous↗
PubMed2005

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.

Administration, Oral↗
PubMed2005

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.

Journal Article↗
PubMed2005

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. METHODS 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.

Aged↗
PubMed2004

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.

Acetylcholine↗
PubMed2004

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.

Adult↗
PubMed2003

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.

Adult↗
PubMed2002

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.

Adult↗
PubMed2002

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.

Adult↗
PubMed2002

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.

Adult↗
PubMed2002

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. METHODS 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.

Algorithms↗
PubMed2001

Dynamics of local pressure-induced cutaneous vasodilation in the human hand.

We recently demonstrated that a pressure-induced vasodilation results from local nonnociceptive stimulation of the skin of the human hand. We aimed to test the hypothesis that this vasodilation was not a short-lived response to a single type of pressure strain, but could be a widely activated and prolonged protective cutaneous response. We studied the dynamics of pressure-induced vasodilation during various ramp changes in local externally applied pressure using laser Doppler flowmetry. Changes from an adjacent control probe were subtracted from pressure-induced local changes. Following an initial transient decrease, continuous 4.4, 5.6, and 11.1 Pa.s(-1) increases of pressure resulted in a secondary increase of blood flow whose amplitude was maximal for 11.1 Pa.s(-1) (22.9 +/- 12.6% above baseline) (mean +/- SEM). The increase in flow was not noted at 16.7 Pa.s(-1). If the 16.7 Pa.s(-1) ramp pressure increase was interrupted at min 2 or 4, a prolonged vasodilation response was found, but not if it was stopped at min 8. When the 16.7 Pa.s(-1) increasing pressure was returned to zero after 4 min of pressure increase (-8.1 +/- 8.9% before pressure removal), vasodilation occurred and reached a maximum of 26.0 +/- 9.6% at 7 min after removal of pressure (P < 0.05 from baseline). Pressure-induced vasodilation is a slow-responding and transient adaptive phenomenon, initiated by a wide range of pressure changes below the range of noxious stimulation. We propose that this response is a protective mechanism without which certain pressure-associated lesions may develop.

Adult↗
PubMed2001

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.

Adult↗
PubMed2001

Pressure measurements at rest and after heavy exercise to detect moderate arterial lesions in athletes.

PURPOSE: This study defined how ankle arterial blood pressure measurements should be analyzed for the detection of moderate arterial disease (asymptomatic while walking). We used external iliac artery endofibrosis as a unique model of an isolated moderate arterial lesion, the role of which in exercise-related pain can be surgically proven. METHODS: Patients who were ambulatory in our institutional referral center were studied. Brachial pressures, ankle pressures, and heart rate were measured simultaneously on all four limbs at rest and after maximal exercise in 108 healthy athletes and 78 patients (among 89 athletes referred for suspicion of endofibrosis) with confirmed or excluded external iliac endofibrosis. For these 78 patients, we calculated systolic ankle pressure change, ankle/brachial index, and deviation from the ankle/brachial index to heart rate regression line (DAHR) that was defined in the 108 healthy athletes. RESULTS: In patients with endofibrosis, ankle/brachial index and ankle pressure were normal at rest. One minute after exercise, areas (mean +/- SE of area) under the receiver operating characteristics curve for the diagnosis of endofibrosis were 0.91 +/- 0.02, 0.91 +/- 0.03, 0.95 +/- 0.02, and 0.96 +/- 0.02 for ankle pressure, pressure change, ankle/brachial index, and DAHR, respectively. For all criteria, area decreased with time in the recovery period. CONCLUSION: After heavy-load exercise, the ankle/brachial index at minute 1 should be used rather than the systolic ankle pressure value or ankle pressure change as a means of improving the efficacy of the detection of endofibrosis in athletes. A 0.66 value of the index at minute 1 after maximal exercise seems an optimal cutoff point for clinical use, providing a 90% sensitivity rate and 87% specificity rate in the diagnosis of moderate arterial lesions. At rest and after 1 minute of recovery, the ankle/brachial index to heart rate relationship should be considered to be an efficient tool for analyzing the results of pressures measurements and improving detection efficiency.

Adult↗
PubMed2001

The influence of topical capsaicin on the local thermal control of skin blood flow in humans.

To test whether heat-sensitive receptors participate in the cutaneous vascular responses to direct heating, we monitored skin blood flow (SkBF; laser Doppler flowmetry) where the sensation of heat was induced either by local warming (T(Loc); Peltier cooling/heating unit) or by both direct warming and chemical stimulation of heat-sensitive nociceptors (capsaicin). In part I, topical capsaicin (0.075 or 0.025%) was applied to 12 cm(2) of skin 1 h before stepwise local warming of untreated and capsaicin-treated forearm skin. Pretreatment with 0.075% capsaicin cream shifted the SkBF/T(Loc) relationship to lower temperatures by an average of 6 +/- 0.8 degrees C (P < 0.05). In part II, we used a combination of topical capsaicin (0.025%) and local warming to evoke thermal sensation at one site and only local warming to evoke thermal sensation at a separate site. Cutaneous vasomotor responses were compared when the temperatures at these two sites were perceived to be the same. SkBF differed significantly between capsaicin and control sites when compared on the basis of actual temperatures, but that difference became insignificant when compared on the basis of the perceived temperatures. These data suggest heat-sensitive nociceptors are important in the cutaneous vasodilator response to local skin warming.

Administration, Topical↗
PubMed2001

Reflex control of the cutaneous circulation after acute and chronic local capsaicin.

To investigate whether local activity of capsaicin-sensitive sensory afferents in the skin has a modulatory role in the reflex cutaneous vasodilator response to hyperthermia in humans, experiments were conducted in two parts. First, low-dose topical capsaicin (0.025%) was administered acutely to stimulate local activity of these afferents. Second, we temporarily desensitized these nerves in a small area of skin using chronic capsaicin treatment (0.075% for 7 days). Each intervention was followed by whole body heating using water-perfused suits and then by local warming to 42 degrees C for assessment of maximum cutaneous vascular conductance. Skin blood flow was measured by laser-Doppler flowmetry and divided by mean arterial pressure (Finapres) for assessment of cutaneous vascular conductance. Maximum vascular conductance was not influenced by either acute or chronic capsaicin treatment (P > 0.10). After acute capsaicin, baseline cutaneous vascular conductance was elevated above that at control sites (25.34 +/- 6.25 vs. 10.57 +/- 2.42%max; P < 0.05). However, internal temperature thresholds for vasodilation were not affected by either acute or chronic capsaicin (P > 0.10). Furthermore, neither acute (control: 112.74 +/- 36.83 vs. acute capsaicin: 96.92 +/- 28.92%max/ degrees C; P > 0.10) nor chronic (control: 142.45 +/- 61.89 vs. chronic capsaicin: 132.12 +/- 52.60%max/ degrees C; P > 0.10) capsaicin administration influenced the sensitivity of the reflex cutaneous vasodilator response. We conclude that local activity of capsaicin-sensitive afferents in the skin does not modify reflex cutaneous vasodilation during hyperthermia.

Administration, Topical↗
PubMed2001

New method of cardiac output measurement using ultrasound velocity dilution in rats.

The aim of this study was to validate a new technique for the measurement of cardiac output (CO) based on ultrasound and dilution (COUD) in anesthetized rats. A transit time ultrasound (TTU) probe was placed around the rat carotid artery, and ultrasound velocity dilution curves were generated on intravenous injections of saline. CO by COUD were calculated from the dilution curves for normal and portal hypertensive rats in which CO was known to be increased. COUD was compared with the radiolabeled microsphere method and with direct aortic TTU flowmetry for baseline CO and drug-induced CO variations. CO in direct aortic TTU flowmetry was the ascending aorta blood flow measured directly by TTU probe (normal use of TTU flowmetry). The reproducibility of COUD within the same animal was also determined under baseline conditions. COUD detected the known CO increase in portal hypertensive rats compared with normal rats. CO values by COUD were correlated with those provided by microsphere technique or direct aortic TTU flowmetry (adjusted r = 0.76, P < 10(-4) and r = 0.79, P < 0.05, respectively). Baseline CO values and terlipressin-induced CO variations were detected by COUD and the other techniques. Intra- and interobserver agreements for COUD were excellent (intraclass r = 0.99 and 0.98, respectively). COUD was reproducible at least 10 times in 20 min. COUD is an accurate and reproducible method providing low-cost, repetitive CO measurements without open-chest surgery. It can be used in rats as an alternative to the microsphere method and to direct aortic flowmetry.

Animals↗