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Y Jammes

Publications and source records attributed to Y Jammes.

At least 19 recordsLinked to original sources

Chronic electrostimulation after nerve repair by self-anastomosis: effects on the size, the mechanical, histochemical and biochemical muscle properties.

This study tests the effects of chronic electrostimulation on denervated/reinnervated skeletal muscle in producing an optimal restoration of size and mechanical and histochemical properties. We compared tibialis anterior muscles in four groups of rats: in unoperated control (C) and 10 weeks following nerve lesion with suture (LS) in the absence of electrostimulation and in the presence of muscle stimulation with either a monophasic rectangular current (LSEm) or a biphasic modulated current (LSEb). The main results were (1) muscle atrophy was reduced in LSEm (-26%) while it was absent in LSEb groups (-8%); (2) the peak twitch amplitude decreased in LS and LSEm but not in LSEb groups, whereas the contraction time was shorter; (3) muscle reinnervation was associated with the emergence of type IIC fibers and proportions of types I, IIA and IIB fibers recovered in the superficial portion of LSEb muscles; (4) the ratio of oxidative to glycolytic activities decreased in the three groups with nerve injury and repair; however, this decrease was more accentuated in LSEm groups. We conclude that muscle electrostimulation following denervation and reinnervation tends to restore size and functional and histochemical properties during reinnervation better than is seen in unstimulated muscle.

Adenosine Triphosphatases↗

Effect of long-term atorvastatin treatment on the electrophysiological and mechanical functions of muscle.

OBJECTIVE: To study alterations in muscle function combining physiological, electrophysiological and metabolic measurements in patients receiving a statin at various dosages during long-term therapy. MATERIAL: A 3-month (D0, D30 and D90) longitudinal physiological and electrophysiological muscle study was performed in 26 patients receiving 10, 40 or 80 mg/day atorvastatin. METHOD: All subjects performed maximal (MVC) and submaximal (60% MVC) isometric thumb adduction, handgrip and knee extension exercises during the recording of surface electromyograms (EMG) of the adductor pollicis (AP), flexor digitorum (FD) and vastus lateralis (VL). The compound muscle potential (M-wave) evoked by direct muscle stimulation was measured at rest and after 60% MVCs and the EMG power spectrum was analyzed during sustained effort. Blood was sampled from an antecubital vein for measurements of pH, lactate and potassium levels after thumb adduction and handgrip exercises. The measurements were repeated on Day 0 (D0), D30 and D90. RESULTS: Atorvastatin did not affect the MVC and endurance time to fatigue. Post-exercise M-wave alterations in the AP began at D30 with the 80 mg/day treatment and there was a reduced or suppressed leftward shift in the EMG power spectrum in the AP and VL with all 3 dosages. In the AP, the EMG changes appeared earlier (D30) with 80 mg/day whereas they only occurred at D90 on the lower dosages. Atorvastatin had no effect on the maximal postexercise variations in pHv and lactate but it significantly reduced the maximal increase in plasma potassium concentration after thumb adduction and handgrip exercise, the effects being only present at D90 on 10 mg/day but occurring as early as D30 with higher dosages. CONCLUSION: A 3-month atorvastatin treatment did not affect the maximal performance of skeletal muscle during voluntary efforts but EMG analysis revealed a reduced muscle excitability and an attenuated adaptation to fatigue. These effects prevailed in muscles containing the largest proportion of slow-oxidative fibers and were associated with a reduced outward flow of potassium.

Anticholesteremic Agents↗

Evidence that free radical generation occurs during scorpion envenomation.

Although it is well established that symptomatology, morbidity and death following scorpion envenomation are due to increases in neurotransmitter release secondary to toxins binding to voltage-sensitive sodium channels, the mechanism by which venom action is involved in damaging heart, liver, lungs and kidneys remains unclear. We hypothesized that scorpion toxins could induce the generation of high levels of free radicals responsible for membrane damage in organs targeted by venom action. We have investigated lipid peroxidation in different organs, through the evaluation of thiobarbituric acid reactive substances (TBARS), after experimental envenomation of rats by toxic fractions of Androctonus australis Hector venom. We have shown that scorpion toxins cause considerable lipid peroxidation in most vital organs. We also evaluated the protective effects of antioxidants in mice injected with lethal doses of toxins. Among the drugs tested, N-acetylcysteine (NAC) was effective in protecting the mice when injected prior to toxin application. However, the free radical scavenging properties of NAC seem less implicated in these protective effects than its ability to increase the fluidity of bronchial secretions. We therefore conclude that free radical generation only plays a minor role in the toxicity of scorpion venom.

Acetylcysteine↗

Chronic fatigue syndrome: assessment of increased oxidative stress and altered muscle excitability in response to incremental exercise.

OBJECTIVES: Because the muscle response to incremental exercise is not well documented in patients suffering from chronic fatigue syndrome (CFS), we combined electrophysiological (compound-evoked muscle action potential, M wave), and biochemical (lactic acid production, oxidative stress) measurements to assess any muscle dysfunction in response to a routine cycling exercise. DESIGN: This case-control study compared 15 CFS patients to a gender-, age- and weight-matched control group (n=11) of healthy subjects. INTERVENTIONS: All subjects performed an incremental cycling exercise continued until exhaustion. MAIN OUTCOME MEASURES: We measured the oxygen uptake (VO2), heart rate (HR), systemic blood pressure, percutaneous O2 saturation (SpO2), M-wave recording from vastus lateralis, and venous blood sampling allowing measurements of pH (pHv), PO2 (PvO2), lactic acid (LA), and three markers of the oxidative stress (thiobarbituric acid-reactive substances, TBARS, reduced glutathione, GSH, and ascorbic acid, RAA). RESULTS: Compared with control, in CFS patients (i) the slope of VO2 versus work load relationship did not differ from control subjects and there was a tendency for an accentuated PvO2 fall at the same exercise intensity, indicating an increased oxygen uptake by the exercising muscles; (ii) the HR and blood pressure responses to exercise did not vary; (iii) the anaerobic pathways were not accentuated; (iv) the exercise-induced oxidative stress was enhanced with early changes in TBARS and RAA and enhanced maximal RAA consumption; and (v) the M-wave duration markedly increased during the recovery period. CONCLUSIONS: The response of CFS patients to incremental exercise associates a lengthened and accentuated oxidative stress together with marked alterations of the muscle membrane excitability. These two objective signs of muscle dysfunction are sufficient to explain muscle pain and postexertional malaise reported by our patients.

Analysis of Variance↗

Increased diaphragmatic strength and tolerance to fatigue after bilateral lung transplantation: an electromyographic study.

We evaluated the diaphragmatic function of seven patients with severe chronic respiratory failure before and after a bilateral lung transplantation (BLT), with follow-up at one year of pulmonary function tests, maximal inspiratory mouth pressure (MIP) and surface diaphragmatic electromyogram (Edi). The patients were asked to sustain target inspiratory pressures at -15, -30, and -50 cmH(2)O. We measured the endurance time (Tlim) to sustain inspiratory efforts and the power spectrum density function of Edi at each inspiratory maneuver. The Edi power spectra was analysed in terms of median frequency (MF), total power (TP) and energies in high-and low-frequency bands (EL and EH). Before BLT, a defect of the diaphragmatic function was evident: MIP was 62+/-7% of the predicted value and the Tlim measured at each inspiratory effort was very short ( 13+/-1 s, 10+/-1 s and 8+/-1 s at pressures of -15, -30, and -50 cmH(2)O, respectively). One month after BLT, the Tlim began to increase at all target inspiratory pressures and at 6 months MIP recovered to normal values. One month after BLT, there was a significant decrease in TP measured at the beginning of each inspiratory efforts and also an increase in the concomitant MF value. BLT markedly accentuated the maximal variations of TP, MF and low-frequency Edi energy. Some hypotheses are raised to explain this dramatic improvement in diaphragmatic function after BLT.

Adolescent↗

Electromyographic signs of neuromuscular fatigue are concomitant with further increase in ventilation during static handgrip.

We questioned if a non-linear increase in ventilation defining a ventilatory threshold (V(Th)) accompanied the electromyographic (EMG) signs of neuromuscular fatigue. Indeed, the intramuscular accumulation of metabolites may activate the afferent nervous pathways responsible for both the 'muscle wisdom' phenomenon and the respiratory centre activation. During inframaximal (50%) handgrip sustained until exhaustion, minute ventilation (V(E)), V(E)/V(O2) and V(E)/V(CO2) ratios were measured simultaneously with surface EMG of the 'flexor digitorum' muscle. V(Th) was defined as a non-linear V(E) increase and/or an abrupt V(E)/V(O2) increase without any concomitant increase in the V(E)/V(CO2) ratio. Handgrip was repeated during complete arterial blood flow interruption in order to suppress any venous return from the exercising forearm. In both control and blood flow interruption conditions, an abrupt increase in the V(E)/V(O2) ratio was measured in the majority of trials (13 of 15 and 14 of 15, respectively) and the EMG signs of neuromuscular fatigue (a decline in median frequency and/or a non-linear increase in low-frequency EMG energies, E(L)) were concomitant with the V(Th) determination. Thus, V(Th) occurs during sustained static contraction and is concomitant with EMG signs of neuromuscular fatigue. Neurogenic factors seem to be responsible for the two responses which persist despite the absence of any release of metabolites in the circulation.

Adult↗

Combined in situ analysis of metabolic and myoelectrical changes associated with electrically induced fatigue.

Electrical muscle stimulation (Mstim) at a low or high frequency is associated with failure of force production, but the exact mechanisms leading to fatigue in this model are still poorly understood. Using 31P magnetic resonance spectroscopy (31PMRS), we investigated the metabolic changes in rabbit tibialis anterior muscle associated with the force decline during Mstim at low (10 Hz) and high (100 Hz) frequency. We also simultaneously recorded the compound muscle mass action potential (M-wave) evoked by direct muscle stimulation, and we analyzed its post-Mstim variations. The 100-Hz Mstim elicited marked M-wave alterations and induced mild metabolic changes at the onset of stimulation followed by a paradoxical recovery of phosphocreatine (PCr) and pH during the stimulation period. On the contrary, the 10-Hz Mstim produced significant PCr consumption and intracellular acidosis with no paradoxical recovery phenomenon and no significant changes in M-wave characteristics. In addition, the force depression was linearly linked to the stimulation-induced acidosis and PCr breakdown. These results led us to conclude that force failure during 100-Hz Mstim only results from an impaired propagation of muscle action potentials with no metabolic involvement. On the contrary, fatigue induced by 10-Hz Mstim is closely associated with metabolic changes with no alteration of the membrane excitability, thereby underlining the central role of muscle energetics in force depression when muscle is stimulated at low frequency. Finally, our results further indicate a reduction of energy cost of contraction when stimulation frequency is increased from 10 to 100 Hz.

Acidosis↗

Effect of muscle electrostimulation on afferent activities from tibialis anterior muscle after nerve repair by self-anastomosis.

Numerous previous studies were devoted to the regeneration of motoneurons toward a denervated muscle after nerve repair by self-anastomosis but, to date, few investigations have evaluated the regeneration of sensory muscle endings. In a previous electrophysiological study (Decherchi et al., 2001) we showed that the functional characteristics of tibialis anterior muscle afferents are affected after self-anastomosis of the peroneal nerve even when the neuromuscular preparation was not chronically stimulated. The present study examines the regeneration of groups I-II (mechanosensitive) and groups III-IV (metabosensitive) muscle afferents by evaluating the recovery of their response to different test agents after self-anastomosis combined or not with chronic muscle stimulation for a 10-weeks period. We compared five groups of rats: C, control; L, nerve lesion without suture; LS, nerve lesion with suture; LSE(m): nerve lesion plus chronic muscle stimulation with a monophasic rectangular current; and LSE(b): nerve lesion plus chronic stimulation with a biphasic current with modulations of pulse duration and frequency, eliciting a pattern of activity resembling that delivered by the nerve to the muscle. Compared to the control group, (1) muscle kept only its original weight in the LSE(b) group, (2) in the LS group the response curve to tendon vibration was shifted toward the highest mechanical frequencies and the response of groups III-IV afferents after fatiguing muscle stimulation lowered, (3) in the LSE(m) group, the pattern of activation of mechanoreceptors by tendon vibrations was altered as in the LS group, and the response of metabosensitive afferents to KCl injections was markedly reduced, (4) in the LSE(b) group, the response to tendon vibration was not modified and the activation of metabosensitive units by increased extracellular potassium chloride concentration was conserved. Both LSE(b) and LSE(m) conditions were ineffective to maintain the post muscle stimulation activation of metabosensitive units as well as their activation by injected lactic acid solutions. Our data indicate that chronic muscle electrostimulation partially favors the recovery of mechano- and metabosensitivity in a denervated muscle and that biphasic modulated currents seem to provide better results.

Action Potentials↗

High or low doses of almitrine bismesylate in ARDS patients responding to inhaled NO and receiving norepinephrine?

OBJECTIVE: To evaluate the effects on oxygenation and pulmonary haemodynamics of almitrine bismesylate (AB) 5 microg/kg per minute and 16 microg/kg per minute in ARDS patients responding to and receiving inhaled NO (iNO) and presenting septic shock requiring norepinephrine, while no difference was observed in a previous trial including iNO responders and nonresponders. DESIGN: Prospective, cohort study. SETTING: Adult medico-surgical intensive care unit of a university hospital. PATIENTS: Fifteen patients with ARDS receiving and responding to iNO (10 ppm) and presenting septic shock requiring norepinephrine (mean 0.5+/-0.45 microg/kg per minute, range 0.08- 2.08). INTERVENTIONS: The protocol consisted of two consecutive phases in a fixed order: continuous intravenous infusion of AB 5 microg/kg per minute for 30 min, and continuous intravenous infusion of AB 16 microg/kg per minute for 30 min. MEASUREMENTS AND MAIN RESULTS: AB 5 microg/kg per minute significantly increased PaO2/FiO2 ( P<0.05) compared with iNO alone [160 (range 77-450) mmHg vs 122 (range 70-225) mmHg]. AB 16 microg/kg per minute produced a greater increase of PaO2/FiO2 ( P<0.05) when compared with 5 microg/kg per minute [227 (range 84-501) mmHg]. AB did not improve shunt at any dose regimen. AB produced an increase in mean pulmonary arterial pressure (MPAP) from 22+/-5 to 25+/-4 mmHg ( P<0.03). MPAP did not significantly increase between the two doses. Pulmonary vascular resistances and other haemodynamic and respiratory parameters were not affected by almitrine bismesylate. CONCLUSIONS: These results suggest that it is possible to obtain a further improvement in oxygenation by increasing AB infusion rate in ARDS patients iNO responders receiving norepinephrine. Due to the potential deleterious effects of AB, this strategy should be used in the most severely hypoxaemic patients.

Administration, Inhalation↗

Effects of chronic hypoxemia on the afferent nerve activities from skeletal muscle.

An acute reduction of the oxygen supply to contracting muscles not only affects their metabolism but also modifies their sensorimotor control through changes in afferent discharge of the group I and group III-IV nerve fibers, the latter playing a pivotal role in the protective mechanisms against muscle fatigue. The effects of chronic hypoxemia on the muscle sensitivity are totally unknown. In the present study, group I fibers (mechanosensory afferents) and group III-IV fibers (mechanosensory and chemosensory afferents) from the anterior tibial muscle were recorded in normoxemic and chronic hypoxemic rats. Hypoxemic rats breathed for 45 d a gas mixture containing 9.5 to 10% O(2) in N(2). The data were compared with those obtained in normoxemic animals of the same age. To activate the different muscle afferents, we used different test agents, including electrically induced fatigue (EIF), KCl, lactic acid injections, as well as tendon vibrations. The conduction velocity of all nerve fibers was significantly (p < 0.01) higher in hypoxemic rats than in the normoxemic group. Chronic hypoxemia significantly depressed the response of the group III-IV muscle afferents to KCl injections and even abolished their response to lactic acid and EIF. However, the response to tendon vibrations of the group I afferents was similar in hypoxemic and normoxemic rats. These results suggest that chronic hypoxemia markedly alters the chemosensitivity of the group III-IV muscle afferents, which may explain the higher fatigability of hypoxemic subjects.

Animals↗

Exercise-induced inflammatory reaction affects electromyographic changes in skeletal muscle during dynamic contractions in humans.

In order to assess the role of exercise-induced inflammatory reactions on electromyographic (EMG) changes in humans, we have recorded, during a 3-min dynamic handgrip exercise at a high strength (112 w), the surface EMG and the compound evoked muscle action potential (M-wave) in control conditions, and this after ingestion of a well known cyclooxygenase blocker i.e. acetylsalicylic acid (ASA), either as a single dose treatment (10 mg/kg) and as a 3-day treatment (30 mg/kg per day). The power spectrum density function of EMG allowed us to compute both the median frequency (MF) and the energies in a low- and a high-frequency band. We estimated the lactic acid concentration from blood samples drawn from an antecubital vein and we noted that its production was not affected by ASA (single dose or 3-day treatment). We observed at the end of exercise that no change in M-wave duration and conduction time occurred though the median frequency always fell. However, we noted that the slope of the MF vs. time regression line was halved after the 3-day ASA treatment which may indicate that inflammatory reactions are elicited by exhausting contractions and affect the EMG changes.

Action Potentials↗

Changes in afferent activities from tibialis anterior muscle after nerve repair by self-anastomosis.

In order to study sensory nerve plasticity after nerve injury and repair, recordings were made from afferent axons innervating the tibialis anterior muscle in rats under several different experimental conditions. In two groups of rats, reinnervation of the denervated tibialis anterior was examined 2.5 months (group A) and 7 months (group B) after section, along with self-anastomosis of the common peroneal nerve. The other rats (group C) were examined 2.5 months after the nerve was cut and ligatured to its stumps to avoid axonal regeneration. No evoked potentials and no activation in response to any test agent were found in group C rats. We found a significant increase in the proportion of group I-II fibers and a significant decrease in group IV fibers in the group B rats when compared with group A (P < 0.05 and P < 0.01) and control animals (P < 0.01 and P < 0.01). A higher conduction velocity was measured in group IV fibers in group B rats when compared with group A (P < 0.01) and the controls (P < 0.01). The proportion of afferent units showing an optimal discharge in response to tendon vibration at 70 Hz (range 0-100 Hz) was higher in groups A and B (72.2 and 80%, respectively) than in the controls (36.8%). The response of muscle afferents to KCl (1-20 mM) and lactic acid (0.5-3 mM) concentrations was markedly depressed in group A rats (P < 0.05), whereas it was restored and even accentuated in group B animals when compared with the controls (P < 0.05). Electrically induced fatigue (3 min, 10 Hz) significantly activated (P < 0.05) muscle afferents only in controls. The present study indicates that after self-anastomosis of a cut hindlimb muscle nerve, sensory innervation was markedly modified in the direction of enhanced mechanosensitivity to high-frequency tendon vibration and depressed metabosensitivity.

Animals↗

Effects of endogenous nitric oxide in activation of group IV muscle afferents.

Based on previous observations that acute hypoxemia, which enhances nitric oxide (NO) production, depresses the activation of group IV afferents after repetitive low-frequency muscle stimulation (MS), we hypothesized that endogenous NO modulates the response of these nerve endings to their specific stimuli. The present study in rabbits examined the effects of a blocker of NO synthase (NG-nitro-L-arginine methyl ester L, L-NAME) and an exogenous NO donor (3-morpholinosydnonimine, SIN-1) on the group IV afferents of tibialis anterior. The efficacy of the two test agents was judged by their effects on systemic blood pressure. L-NAME markedly elevated (+46%) the resting discharge rate of group IV afferents but abolished their activation after repetitive MS. After SIN-1 injection, there was a transient decrease in blood pressure, which correlated well with a lowered resting discharge rate of group IV afferents. SIN-1 infusion caused a stable reduction of blood pressure; the resting afferent nerve discharge rate began first to decrease but then recovered control mean values. SIN-1 infusion abolished the activation of group IV afferents after MS. This study indicates that endogenous NO production in a resting or contracting muscle attenuates the baseline activity of group IV muscle afferents and their activation after repetitive muscle contractions.

Animals↗

Effects of acute hypoxemia on force and surface EMG during sustained handgrip.

Data on the consequences of acute hypoxemia on the strength of contraction are often contradictory. In healthy subjects, we tested the effects of hypoxemia (PaO(2) = 56 mmHg), maintained for a 30-min period, on static handgrip elicited by voluntary effort or direct electrical muscle stimulation, in order to separate the consequences of hypoxemia on central or peripheral factors, respectively. Force was measured during maximal voluntary contractions (MVCs), 60% MVCs sustained until exhaustion, and 1-min periods of electrical muscle stimulation at 60 HZ. The evoked compound muscle action potential (M wave) was recorded in resting muscle and after each period of 60-HZ stimulation or sustained 60% MVC. Power spectrum analysis of surface electromyogram (EMG) was performed during sustained 60% MVC. Compared to normoxemia, acute hypoxemia lowered MVC (-12%, P < 0.01) but enhanced (+38%, P < 0.01) the peak force elicited by electrical muscle stimulation. In resting muscle, hypoxemia had no influence on the M-wave amplitude but lengthened the neuromuscular transmission time(+740 micros, P < 0.05). Hypoxemia did not alter the M wave measured after 60 HZ stimulation and 60% MVC. During sustained 60% MVC, hypoxemia markedly depressed the EMG changes, abolishing the leftward shift of power spectra. These data show that acute hypoxemia reduces MVC through depression of the central drive, whereas it improves the peripheral muscle response to electrical stimulation. In addition, hypoxemia reduces the recruitment of slow firing motor unit, which are highly oxygen-dependent. This could constitute an adaptative muscle response to a reduced oxygen supply.

Action Potentials↗

Is a short trial of prone positioning sufficient to predict the improvement in oxygenation in patients with acute respiratory distress syndrome?

OBJECTIVE: To determine whether a 1-h trial of prone positioning is sufficient to identify responders. DESIGN: Prospective clinical cohort study in a medico-surgical ICU in a teaching hospital. PATIENTS: 49 patients with acute respiratory distress syndrome. INTERVENTIONS: A 6-h period of prone positioning. MEASUREMENTS AND RESULTS: Baseline measurements (blood gas analysis and respiratory parameters) were evaluated in supine position just prior to turning the patients prone. Measurements were then repeated 1 h after the beginning of prone positioning (PP1h) and at the end of the 6-h period of prone positioning (PP6h). The last measurements were performed 1 h after repositioning the patients supine. Prone position induced an increase in the PaO2/FIO2 ratio (p < 0.001). A response (increase in PaO2/FIO2 ratio of at least 20 % at PP1h and/or at PP6h) was observed in 37 of 49 patients (76%). Twenty-seven of these patients (73%) were responders at PP1h while 10 (27%) were responders only at PP6h- In all, two-thirds of the patients were considered persistent responders. However, whereas the PaO2/FIO2 ratio decreased significantly 1 h after repositioning the fast responders supine, the PaO2/ FIO2 ratio remained unchanged after repositioning slow responders. CONCLUSIONS: A short-term trial of prone positioning does not appear a sufficient method to identify patients who would benefit from the postural treatment.

APACHE↗

Operation Everest III (Comex'97): the effect of simulated sever hypobaric hypoxia on lipid peroxidation and antioxidant defence systems in human blood at rest and after maximal exercise.

Eight subjects were placed in a decompression chamber for 31 days at pressures from sea level (SL) to 8848 m altitude equivalent. Whole blood lipid peroxidation (LP) was increased at 6000 m by a mean of 23% (P<0.05), at 8000 m by 79% (P<0.01) and at 8848 m by 94% (P<0.01). (All figures are means.) Two days after return to sea level (RSL), it remained high, by 81% (P<0.01), while corresponding erythrocyte GSH/GSSG ratios decreased by 31, 46, 49, 48%, respectively (each P<0.01). Erythrocyte SOD and plasma ascorbate did not change significantly. At sea level, maximal exercise induced a 49% increase in LP (P<0.01), and a 27% decrease in erythrocyte GSH/GSSG ratio relative to resting values (P<0.05). At 6000 m, the LP was enhanced further from 23 (P<0.05) to 66% (P<0.01), and after RSL from 81 (P<0.01) to 232% (P<0.01), while pre-exercise GSH/GSSG ratios did not change significantly. Exercise did not change plasma ascorbate relative to sea level or to 6000 m, but decreased after RSL by 32% (P<0.01). These findings suggest that oxidative stress is induced by prolonged hypobaric hypoxia, and is maintained by rapid return to sea level, similar to the post-hypoxic re-oxygenation process. It is increased by physical exercise.

Acclimatization↗

The changes in leg blood flow during and after mild or severe acute hypoxaemia in healthy humans.

The present study examines the leg blood flow changes in resting healthy humans during and after a 10-min period of mild (PaO2=5.60 kPa) or severe hypoxaemia (PaO2=4.53 kPa) induced by breathing hypoxic gas mixtures. A Colour Duplex Scan system allowed to measure the cross-sectional area (CSA) and mean blood flow (Q) in a femoral artery (FA) and a femoral vein (FV) and also in an artery supplying leg muscles (medial gastrocnemius artery, MGA). During the mild as well as the severe hypoxaemia and their recovery periods, no significant variations of Q and CSA occurred in FA and FV. During the mild hypoxaemia and the first 10 min of the recovery period, Q and CSA of MGA increased (maximal changes: +84 and +20%, respectively). By contrast, a marked Q decrease and a reduced CSA were measured in MGA during the severe hypoxaemia (-67 and -60%, respectively). This reduced muscle blood flow was followed by a vasodilatation (CSA increase = +30%), which began 10 min after the hypoxaemia ended and persisted for a further 10-min period. This study shows that the time course of muscle blood flow changes in response to acute hypoxaemia depends on the PaO2 level. Reverse effects were measured during the mild or the severe hypoxaemia, whereas a post-hypoxaemic vasodilatation occurred in all circumstances.

Adult↗