Evaluation of computed tomography in the diagnosis of ultrasound-proven diaphragm dysfunction.

INTRODUCTION: Computed tomography (CT) is routinely employed on the evaluation of dyspnea, yet limited data exist on its assessment of diaphragmatic muscle. This study aimed to determine the capability of CT in identifying structural changes in the diaphragm among patients with ultrasound-confirmed diaphragmatic dysfunction. METHODS: Diaphragmatic ultrasounds conducted between 2018 and 2021 at our center in Marseille, France, were retrospectively collected. Diaphragmatic pillars were measured on CT scans at the L1 level and the celiac artery. Additionally, the difference in height between the two diaphragmatic domes in both diaphragmatic dysfunction cases and controls was measured and compared. RESULTS: A total of 65 patients were included, comprising 24 with diaphragmatic paralysis, 13 with diaphragmatic weakness, and 28 controls. In the case group (paralysis and weakness) with left dysfunctions (n = 24), the CT thickness of the pillars at the level of L1 and the celiac artery was significantly thinner compared with controls (2.0 mm vs. 7.4 mm and 1.8 mm vs. 3.1 mm, p < 0.001 respectively). Significantly different values were observed for paralysis (but not weakness) in the right dysfunction subgroup (n = 15) (2.6 mm vs. 7.4 mm and 2.2 mm vs. 3.8 mm, p < 0.001 respectively, for paralysis vs. controls). Regardless of the side of dysfunction, a significant difference in diaphragmatic height was observed between cases and controls (7.70 cm vs. 1.16 cm and 5.51 cm vs. 1.16 cm, p < 0.001 for right and left dysfunctions, respectively). Threshold values determined through ROC curve analyses for height differences between the two diaphragmatic domes, indicative of paralysis or weakness in the right dysfunctions, were 4.44 cm and 3.51 cm, respectively. Similarly for left dysfunctions, the thresholds were 2.70 cm and 2.48 cm, respectively, demonstrating good performance (aera under the curve of 1.00, 1.00, 0.98, and 0.79, respectively). CONCLUSION: In cases of left diaphragmatic dysfunction, as well as in paralysis associated with right diaphragmatic dysfunction, CT revealed thinner pillars. Additionally, a notable increase in the difference in diaphragmatic height demonstrated a strong potential to identify diaphragmatic dysfunction, with specific threshold values.

Ultrasound evaluation of diaphragmatic function in patients with idiopathic pulmonary fibrosis: a retrospective observational study.

INTRODUCTION: The diaphragm function assessed by ultrasound has been well-studied in COPD, asthma, and intensive care. However, there are only a few studies on diffuse interstitial lung disease, while dyspnea and quality of life are major issues in the management that may depend on the diaphragm. METHODS: We retrospectively included idiopathic pulmonary fibrosis (IPF) patients followed in our center (Marseille, France) between January 2020 and February 2023 who underwent diaphragmatic ultrasound. Our objectives were to describe the diaphragmatic function of IPFs compared to healthy controls and to correlate with clinical, functional, and lung density on CT-scan. RESULTS: 24 IPF patients and 157 controls were included. The diaphragmatic amplitude in IPF was increased at rest (median of 2.20 cm vs 1.88 cm on the right, p < 0.007, and 2.30 cm vs 1.91 cm on the left, p < 0.03, in IPF and controls respectively) and decreased in deep breathing (median of 4.85 cm vs 5.45 cm on the right, p < 0.009, and 5.10 cm vs 5.65 cm on the left, p < 0.046, in IPF and controls respectively). Diaphragmatic thickness was significantly reduced at rest on the right side (median of 1.75 mm vs 2.00 mm, p < 0.02, in IPF and controls respectively) and in deep breathing on both sides compared to controls (mean of 3.82 mm vs 4.15 mm on the right, p < 0.02, and 3.53 mm vs 3.94 mm, on the left, p < 0.009, in IPF and controls respectively). Diaphragmatic amplitude in deep breathing was moderate to strongly correlated with FVC, DLCO, and 6MWT and negatively correlated with the dyspnea and lung density on CT scan. CONCLUSION: The diaphragmatic amplitude and thickness were impaired in IPF compared to controls. Diaphragmatic amplitude is the parameter best correlated with clinical, functional, and lung density criteria. Further studies are needed to determine if diaphragmatic amplitude can be a prognostic factor in IPF.

Ultrasound assessment of the respiratory system using diaphragm motion-volume indices.

Background: Although previous studies have determined limit values of normality for diaphragm excursion and thickening, it would be beneficial to determine the normal diaphragm motion-to-inspired volume ratio that integrates the activity of the diaphragm and the quality of the respiratory system. Methods: To determine the normal values of selected ultrasound diaphragm motion-volume indices, subjects with normal pulmonary function testing were recruited. Ultrasound examination recorded diaphragm excursion on both sides during quiet breathing and deep inspiration. Diaphragm thickness was also measured. The inspired volumes of the corresponding cycles were systematically recorded using a spirometer. The indices were calculated using the ratio excursion, or percentage of thickening, divided by the corresponding breathing volume. From this corhort, normal values and limit values for normality were determined. These measurements were compared to those performed on the healthy side in patients with hemidiaphragm paralysis because an increase in hemidiaphragm activity has been previously demonstated in such circumstances. Results: A total of 122 subjects (51 women, 71 men) with normal pulmonary function were included in the study. Statistical analysis revealed that the ratio of excursion, or percentage of thickening, to inspired volume ratio significantly differed between males and females. When the above-mentioned indices using excursion were normalized by body weight, no gender differences were found. The indices differed between normal respiratory function subjects and patients with hemidiaphragm paralysis (27 women, 41 men). On the paralyzed side, the average ratio of the excursion divided by the inspired volume was zero. On the healthy side, the indices using the excursion and the percentage of thickening during quiet breathing or deep inspiration were significantly increased comparedto patients with normal lung function. According to the logistic regression analysis, the most relevant indice appeared to be the ratio of the excursion measured during quiet breathing to the inspired volume. Conclusion: The normal values of the diaphragm motion-volume indices could be useful to estimate the performance of the respiratory system. Proposed indices appear suitable in a context of hyperactivity.

A Literature Review: ECG-Based Models for Arrhythmia Diagnosis Using Artificial Intelligence Techniques.

In the health care and medical domain, it has been proven challenging to diagnose correctly many diseases with complicated and interferential symptoms, including arrhythmia. However, with the evolution of artificial intelligence (AI) techniques, the diagnosis and prognosis of arrhythmia became easier for the physicians and practitioners using only an electrocardiogram (ECG) examination. This review presents a synthesis of the studies conducted in the last 12 years to predict arrhythmia's occurrence by classifying automatically different heartbeat rhythms. From a variety of research academic databases, 40 studies were selected to analyze, among which 29 of them applied deep learning methods (72.5%), 9 of them addressed the problem with machine learning methods (22.5%), and 2 of them combined both deep learning and machine learning to predict arrhythmia (5%). Indeed, the use of AI for arrhythmia diagnosis is emerging in literature, although there are some challenging issues, such as the explicability of the Deep Learning methods and the computational resources needed to achieve high performance. However, with the continuous development of cloud platforms and quantum calculation for AI, we can achieve a breakthrough in arrhythmia diagnosis.

Muscle metaboreflex activation during hypercapnia modifies nonlinear heart rhythm dynamics, increasing the complexity of the sinus node autonomic regulation in humans.

Muscle metaboreflex activation during hypercapnia leads to enhanced pressive effects that are poorly understood while autonomic responses including baroreflex function are not documented. Thus, we assessed heart rate variability (HRV) that is partly due to autonomic influences on sinus node with linear tools (spectral analysis of instantaneous heart period), baroreflex set point and sensitivity with the heart period-arterial pressure transfer function and sequences methods, and system coupling through the complexity of RR interval dynamics with nonlinear tools (Poincaré plots and approximate entropy (ApEn)). We studied ten healthy young men at rest and then during muscle metaboreflex activation (MMA, postexercise muscle ischemia) and hypercapnia (HCA, PetCO2 = + 10 mmHg from baseline) separately and combined (MMA + HCA). The strongest pressive responses were observed during MMA + HCA, while baroreflex sensitivity was similarly lowered in the three experimental conditions. HRV was significantly different in MMA + HCA compared to MMA and HCA separately, with the lowest total power spectrum (p < 0.05), including very low frequency (p < 0.05), low frequency (p < 0.05), and high frequency (tendency) power spectra decreases, and the lowest Poincaré plot short-term variability index (SD1): SD1 = 36.2 ms (MMA + HCA) vs. SD1 = 43.1 ms (MMA, p < 0.05) and SD1 = 46.1 ms (HCA, p < 0.05). Moreover, RR interval dynamic complexity was significantly increased only in the MMA + HCA condition (ApEn increased from 1.04 ± 0.04, 1.07 ± 0.02, and 1.05 ± 0.03 to 1.10 ± 0.03, 1.13 ± 0.04, and 1.17 ± 0.03 in MMA, HCA, and MMA + HCA conditions, respectively; p < 0.01). These results suggest that in healthy young men, muscle metaboreflex activation during hypercapnia leads to interactions that reduce parasympathetic influence on the sinus node activity but complexify its dynamics.

Diaphragm dysfunction after severe COVID-19: An ultrasound study.

Background: SARS-CoV-2 infection can impair diaphragm function at the acute phase but the frequency of diaphragm dysfunction after recovery from COVID-19 remains unknown. Materials and methods: This study was carried out on patients reporting persistent respiratory symptoms 3-4 months after severe COVID-19 pneumonia. The included patients were selected from a medical consultation designed to screen for recovery after acute infection. Respiratory function was assessed by a pulmonary function test, and diaphragm function was studied by ultrasonography. Results: In total, 132 patients (85M, 47W) were recruited from the medical consultation. During the acute phase of the infection, the severity of the clinical status led to ICU admission for 58 patients (44%). Diaphragm dysfunction (DD) was detected by ultrasonography in 13 patients, two of whom suffered from hemidiaphragm paralysis. Patients with DD had more frequently muscle pain complaints and had a higher frequency of prior cardiothoracic or upper abdominal surgery than patients with normal diaphragm function. Pulmonary function testing revealed a significant decrease in lung volumes and DLCO and the dyspnea scores (mMRC and Borg10 scores) were significantly increased in patients with DD. Improvement in respiratory function was recorded in seven out of nine patients assessed 6 months after the first ultrasound examination. Conclusion: Assessment of diaphragm function by ultrasonography after severe COVID-19 pneumonia revealed signs of dysfunction in 10% of our population. In some cases, ultrasound examination probably discovered an un-recognized pre-existing DD. COVID-19 nonetheless contributed to impairment of diaphragm function. Prolonged respiratory physiotherapy led to improvement in respiratory function in most patients. Clinical trial registration: [www.cnil.fr], identifier [#PADS20-207].

A filter approach for feature selection in classification: application to automatic atrial fibrillation detection in electrocardiogram recordings.

BACKGROUND: In high-dimensional data analysis, the complexity of predictive models can be reduced by selecting the most relevant features, which is crucial to reduce data noise and increase model accuracy and interpretability. Thus, in the field of clinical decision making, only the most relevant features from a set of medical descriptors should be considered when determining whether a patient is healthy or not. This statistical approach known as feature selection can be performed through regression or classification, in a supervised or unsupervised manner. Several feature selection approaches using different mathematical concepts have been described in the literature. In the field of classification, a new approach has recently been proposed that uses the [Formula: see text]-metric, an index measuring separability between different classes in heart rhythm characterization. The present study proposes a filter approach for feature selection in classification using this [Formula: see text]-metric, and evaluates its application to automatic atrial fibrillation detection. METHODS: The stability and prediction performance of the [Formula: see text]-metric feature selection approach was evaluated using the support vector machine model on two heart rhythm datasets, one extracted from the PhysioNet database and the other from the database of Marseille University Hospital Center, France (Timone Hospital). Both datasets contained electrocardiogram recordings grouped into two classes: normal sinus rhythm and atrial fibrillation. The performance of this feature selection approach was compared to that of three other approaches, with the first two based on the Random Forest technique and the other on receiver operating characteristic curve analysis. RESULTS: The [Formula: see text]-metric approach showed satisfactory results, especially for models with a smaller number of features. For the training dataset, all prediction indicators were higher for our approach (accuracy greater than 99% for models with 5 to 17 features), as was stability (greater than 0.925 regardless of the number of features included in the model). For the validation dataset, the features selected with the [Formula: see text]-metric approach differed from those selected with the other approaches; sensitivity was higher for our approach, but other indicators were similar. CONCLUSION: This filter approach for feature selection in classification opens up new methodological avenues for atrial fibrillation detection using short electrocardiogram recordings.

Mental Workload Alters Heart Rate Variability, Lowering Non-linear Dynamics.

Mental workload is known to alter cardiovascular function leading to increased cardiovascular risk. Nevertheless, there is no clear autonomic nervous system unbalance to be quantified during mental stress. We aimed to characterize the mental workload impact on the cardiovascular function with a focus on heart rate variability (HRV) non-linear indexes. A 1-h computerized switching task (letter recognition) was performed by 24 subjects while monitoring their performance (accuracy, response time), electrocardiogram and blood pressure waveform (finger volume clamp method). The HRV was evaluated from the beat-to-beat RR intervals (RRI) in time-, frequency-, and informational- domains, before (Control) and during the task. The task induced a significant mental workload (visual analog scale of fatigue from 27 ± 26 to 50 ± 31 mm, p < 0.001, and NASA-TLX score of 56 ± 17). The heart rate, blood pressure and baroreflex function were unchanged, whereas most of the HRV parameters markedly decreased. The maximum decrease occurred during the first 15 min of the task (P1), before starting to return to the baseline values reached at the end of the task (P4). The RRI dimension correlation (D2) decrease was the most significant (P1 vs. Control: 1.42 ± 0.85 vs. 2.21 ± 0.8, p < 0.001) and only D2 lasted until the task ended (P4 vs. Control: 1.96 ± 0.9 vs. 2.21 ± 0.9, p < 0.05). D2 was identified as the most robust cardiovascular variable impacted by the mental workload as determined by posterior predictive simulations (p = 0.9). The Spearman correlation matrix highlighted that D2 could be a marker of the generated frustration (R = -0.61, p < 0.01) induced by a mental task, as well as the myocardial oxygen consumption changes assessed by the double product (R = -0.53, p < 0.05). In conclusion, we showed that mental workload sharply lowered the non-linear RRI dynamics, particularly the RRI correlation dimension.

Heart rhythm characterization through induced physiological variables.

Atrial fibrillation remains a major cause of morbi-mortality, making mass screening desirable and leading industry to actively develop devices devoted to automatic AF detection. Because there is a tendency toward mobile devices, there is a need for an accurate, rapid method for studying short inter-beat interval time series for real-time automatic medical monitoring. We report a new methodology to efficiently select highly discriminative variables between physiological states, here a normal sinus rhythm or atrial fibrillation. We generate induced variables using the first ten time derivatives of an RR interval time series and formally express a new multivariate metric quantifying their discriminative power to drive state variable selection. When combined with a simple classifier, this new methodology results in 99.9% classification accuracy for 1-min RR interval time series (n = 7,400), with heart rate accelerations and jerks being the most discriminant variables. We show that the RR interval time series can be drastically reduced from 60 s to 3 s, with a classification accuracy of 95.0%. We show that heart rhythm characterization is facilitated by induced variables using time derivatives, which is a generic methodology that is particularly suitable to real-time medical monitoring.

Endogenous adenosine release is involved in the control of heart rate in rats.

Intravenous (i.v.) injections of adenosine exert marked effects on heart rate (HR) and arterial blood pressure (BP), but the role of an endogenous adenosine release by vagal stimulation has not been evaluated. In anaesthetized rats, we examined HR and BP changes induced by 1 min electrical vagal stimulation in the control condition, and then after i.v. injections of (i) atropine, (ii) propranolol, (iii) caffeine, (iv) 8 cyclopentyl-1,3-dipropylxanthine (DPCPX), or (v) dipyridamole to increase the plasma concentration of adenosine (APC). APC was measured by chromatography in the arterial blood before and at the end of vagal stimulation. The decrease in HR in the controls during vagal stimulation was markedly attenuated, but persisted after i.v. injections of atropine and propranolol. When first administered, DPCPX modestly but significantly reduced the HR response to vagal stimulation, but this disappeared after i.v. caffeine administration. Both the HR and BP responses were significantly accentuated after i.v. injection of dipyridamole. Vagal stimulation induced a significant increase in APC, proportional to the magnitude of HR decrease. Our data suggest that the inhibitory effects of electrical vagal stimulations on HR and BP were partly mediated through the activation of A1 and A2 receptors by an endogenous adenosine release. Our experimental data could help to understand the effects of ischemic preconditioning, which are partially mediated by adenosine.

Cardiovascular responses to forearm muscle metaboreflex activation during hypercapnia in humans.

We characterized the cardiovascular responses to forearm muscle metaboreflex activation during hypercapnia. Ten healthy males participated under three experimental conditions: 1) hypercapnia (HCA, PetCO2 : +10 mmHg, by inhalation of a CO2-enriched gas mixture); 2) muscle metaboreflex activation (MMA, by 5 min of local circulatory occlusion after 1 min of 50% maximum voluntary contraction isometric handgrip under normocapnia); and 3) HCA+MMA. We measured mean arterial pressure (MAP), heart rate (HR), and cardiac output (CO); calculated stroke volume (SV), and total peripheral resistance (TPR); and evaluated myocardial oxygen consumption (MV̇o2) and cardiac work (CW) noninvasively. MAP increased in the three experimental conditions but HCA+MMA led to the highest MAP, CO, and HR. Moreover, HCA+MMA increased SV and was associated with the highest MV̇o2 and CW. HCA and MMA exhibited inhibitory interactions with MAP, HR, TPR, MV̇o2, and CW, increases of which were smaller during HCA+MMA than the sum of the increases during HCA and MMA alone (MAP: +28 ± 2 vs. +34 ± 2 mmHg, P < 0.001; HR: +15 ± 2 vs. +22 ± 3 bpm, P < 0.01; TPR: +1.1 ± 1.4 vs. +3.0 ± 1.5 mmHg·l·min(-1), P < 0.05; MV̇o2: +50.25 ± 4.74 vs. +59.48 ± 5.37 mmHg·min(-1)·10(-2), P < 0.01; CW: +59.10 ± 7.52 vs. +63.67 ± 7.71 ml mmHg·min(-1)·10(-4), P < 0.05). Oppositely, HCA and MMA interactions were linearly additive for CO (+2.3 ± 0.4 l/min) and SV (+13 ± 4 ml). We showed that muscle metaboreflex and hypercapnia interact in healthy humans, reducing vasoconstriction but enhancing SV.

Cardiopulmonary response to exercise in COPD and overweight patients: relationship between unloaded cycling and maximal oxygen uptake profiles.

Cardiopulmonary response to unloaded cycling may be related to higher workloads. This was assessed in male subjects: 18 healthy sedentary subjects (controls), 14 hypoxemic patients with chronic obstructive pulmonary disease (COPD), and 31 overweight individuals (twelve were hypoxemic). They underwent an incremental exercise up to the maximal oxygen uptake (VO2max), preceded by a 2 min unloaded cycling period. Oxygen uptake (VO2), heart rate (HR), minute ventilation (VE), and respiratory frequency (fR) were averaged every 10 s. At the end of unloaded cycling period, HR increase was significantly accentuated in COPD and hypoxemic overweight subjects (resp., +14 ± 2 and +13 ± 1.5 min(-1), compared to +7.5 ± 1.5 min(-1) in normoxemic overweight subjects and +8 ± 1.8 min(-1) in controls). The fR increase was accentuated in all overweight subjects (hypoxemic: +4.5 ± 0.8; normoxemic: +3.9 ± 0.7 min(-1)) compared to controls (+2.5 ± 0.8 min(-1)) and COPDs (+2.0 ± 0.7 min(-1)). The plateau VE increase during unloaded cycling was positively correlated with VE values measured at the ventilatory threshold and VO2max. Measurement of ventilation during unloaded cycling may serve to predict the ventilatory performance of COPD patients and overweight subjects during an exercise rehabilitation program.

Inter-individual differences in breathing pattern at high levels of incremental cycling exercise in healthy subjects.

Interindividual differences in the rate of changes in tidal volume (V(T)) and respiratory frequency (f(R)) were examined during a maximal incremental cycling exercise. The gain of the inspiratory off-switch reflex was inferred from the V(T) vs. inspiratory duration (T(i)) relationship. Some subjects also executed a static handgrip exercise, used as a "non-dynamic" exercise trial to study patterning of breathing. Above the ventilatory threshold (V(Th)), two patterns of response were identified: in group 1, the rate of change in V(T) significantly increased, while in group 2 the breakpoint of ventilation solely resulted from f(R) increase. After the respiratory compensation point, a tachypnoeic response always occurred. A leftward shift of the V(T) vs. Ti relationship, i.e., an inspiratory off-switch reflex, was measured during the handgrip in group 2 subjects as well as marked f(R) variations. Our study identifies two different patterns of breathing after the V(Th). The subjects who present a tachypnoeic response to exercise above the V(Th) have a higher sensitivity to pulmonary inflation and their tachypnoeic response was ubiquitous during a maximal handgrip test.

The mechanisms of the widespread production of phosphorylated HSP25 after fatiguing muscle stimulation.

We previously showed that a widespread heat shock protein (HSP) response to fatigue of a single hindlimb muscle was responsible for a global adaptive response to an acute localized stress. We also demonstrated that the HSP response resulted from the activation of nerve afferents from the stimulated muscle. However, we did not examine the role played by the different muscle afferents or the efferent arm of HSP response. In the present study we measured the changes in phosphorylated HSP25 (pHSP25) levels in resting hindlimb muscles and the diaphragm, kidney and brain in response to a fatiguing stimulation of one tibialis anterior muscle that was repeated in five series of experiments: (1) intact muscle innervation, (2) during the selective procaine block of conduction in group IV muscle afferents, (3) after muscle nerve transection to suppress all the sensory messages, and under pharmacological blockade of the (4) alpha-adrenergic or (5) glutamatergic neurotransmission. The data showed that: (1) the pHSP25 response in hindlimb muscles resulted from the stimulation of both group III and IV muscle afferents while the pHSP25 response in the diaphragm, kidney and brain resulted from the sole activation of the group IV fibres, and (2) the blockade of alpha-adrenergic, but not glutamatergic, neurotransmission suppressed the pHSP25 response in all explored tissues except the brain. The present study highlights the role played by the group III and IV muscle afferents in the fatigue-induced pHSP25 response and shows that the sympathetic nerve supply to the muscles and kidney represents the efferent arm of the pHSP25 activation. However, the pHSP25 changes in the brain cannot be explained by the pathways investigated here.

Exercise-induced oxidative stress influences the motor control during maximal incremental cycling exercise in healthy humans.

We hypothesized that the changes in blood oxidant/antioxidant status during incremental maximal cycling exercise could affect the motor drive to leg muscles. Indeed, the oxygen free radicals activate the metabosensitive muscle afferents which are suspected to elicit an adaptive motor response delaying fatigue. Fifteen healthy subjects performed an incremental cycling exercise reaching the maximal oxygen uptake (VO2) during which venous blood was repeatedly sampled to measure a marker of lipid peroxidation (TBARS), an antioxidant (reduced ascorbic acid, RAA), and the ischaemia-modified albumin (IMA). The surface EMG of rectus femoris was recorded and the median frequency (MF) of power spectrum was computed. Our main results are: 1) TBARS increased in 7/15 subjects, RAA decreased in 7/15 and IMA increased in 13/15 at VO2max; 4) the MF decrease was correlated to maximal end-exercise IMA increase and RAA decrease. During maximal cycling exercise, the adaptive motor response to cycling closely depends on the magnitude of exercise-induced oxidative stress.

Effect of voluntary hypocapnic hyperventilation on cutaneous circulation in resting heated humans.

Hypocapnia attenuates the sweat response normally seen in hyperthermic resting subjects, but its effect on the blood flow response in their nonglabrous skin under the same hyperthermic conditions remains unclear. In the present study, we investigated whether hypocapnia induced by voluntary hyperventilation affects the blood flow response to heat stress in the nonglabrous skin of resting humans. Nine healthy male subjects were passively heated using legs-only hot water immersion and a water-perfused suit, which caused esophageal temperature (T(es)) to increase by as much as 1.0°C. During normothermia and at +0.6°C T(es) and +1.0°C T(es), the subjects performed two voluntary 7-min hyperventilation (minute ventilation = 40 l/min) trials (hypocapnic and eucapnic) in random order. End-tidal CO(2) pressure was reduced by 23-25 torr during hypocapnic hyperventilation, but it was maintained at the spontaneous breathing level during eucapnic hyperventilation. Cutaneous blood flow was evaluated as the cutaneous red blood cell flux in the forearm (CBF(forearm)) or forehead (CBF(forehead)) and was normalized to the normothermic spontaneous breathing value. Hypocapnic hyperventilation at +0.6°C T(es) was associated with significantly reduced CBF(forearm), compared with eucapnic hyperventilation, after 5-7 min of hyperventilation (395 to 429 vs. 487 to 525% baseline, P < 0.05). No significant difference in CBF(forehead) was seen during hypocapnic hyperventilation compared with eucapnic hyperventilation at +0.6°C T(es) or +1.0°C T(es). These results suggest that in resting humans, hypocapnia achieved through voluntary hyperventilation attenuates the increase in cutaneous blood flow elicited by moderate heat stress in the nonglabrous skin of the forearm, but not the forehead.

Fatiguing stimulation of one skeletal muscle triggers heat shock protein activation in several rat organs: the role of muscle innervation.

We hypothesised that activation of muscle afferents by fatigue triggers a widespread activation of heat shock proteins (HSPs) in resting muscles and different organs. In anaesthetised rats, HSP25 and HSP70 levels were determined in both tibialis anterior (TA) and extensor digitorum longus (EDL) muscles and in the diaphragm, kidney and brain by ELISA, which mostly identifies phosphorylated HSP, and western blotting. One TA muscle was electrically stimulated and tissues were sampled 10 or 60 min after the stimulation had ended. The nerve supply to the stimulated TA or its counterpart in the contralateral limb was left intact or suppressed. In control rats, no muscle stimulation was performed and tissues were sampled at the same time points (10 or 60 min). After TA stimulation, ELISA showed an increased HSP25 content in the contralateral TA, EDL and diaphragm at 10 min but not at 60 min, and HSP70 increased in all sampled tissues at 60 min. Western blotting did not show any changes in HSP25 and HSP70 at 10 min, while at 60 min HSP25 increased in all sampled tissues except the brain and HSP70 was elevated in all tissues. Denervation of the contralateral non-stimulated limb suppressed HSP changes in TA and after denervation of the stimulated TA the widespread activation of HSPs in other organs was absent. Our data suggest that fatigue-induced activation of skeletal muscle afferents triggers an early increase in phosphorylated HSP25 in muscles and a delayed elevation of non-phosphorylated HSP25 and HSP70 in skeletal and respiratory muscles, kidney and brain.

[Burnout syndrome: a "true" cardiovascular risk factor]. / Syndrome de burnout : un « vrai ¼ facteur de risque cardiovasculaire.

The burnout syndrome is characterized by emotional exhaustion, depersonalization and reduced personal accomplishment in individuals professionally involved with others. The burnout syndrome is poorly recognized, particularly in France, as a distinct nosology from adaptation troubles, stress, depression, or anxiety. Several tools quantifying burnout and emotional exhaustion exist, the most spread is the questionnaire called Maslach Burnout Inventory. The burnout syndrome alters cardiovascular function and its neuroregulation by autonomic nervous system and is associated with: increased sympathetic tone to heart and vessels after mental stress, lowered physiological post-stress vagal rebound to heart, and lowered arterial baroreflex sensitivity. Job strain as burnout syndrome seems to be a real independent cardiovascular risk factor. Oppositely, training to manage emotions could increase vagal tone to heart and should be cardio-protective.

Zeolites are effective ROS-scavengers in vitro.

We report on the use of zeolites to limit the effects of reactive oxygen species (ROS) on human albumin under in vitro conditions. Zeolites of different structure type, channel size, channel polarity, and charge-compensating cation were screened for the elimination of ROS, notably HO(·), resulting from the Fenton reaction. A test based on ischemia-modified albumin (IMA) was used as a marker to monitor the activity of HO(·) after co-exposure of human serum to these zeolites. Two commercial zeolites, faujasite (FAU 13×, channel opening 0.74×0.74 nm with Na(+) as charge-compensating cation) and ferrierite (FER, channel opening 0.54×0.42 nm with H(+) as charge-compensating cation), were found to reduce IMA formation by more than 65% due to removal of HO(·) relative to reference values. It was established that partial ion exchange of the zeolites' respective charge-compensating cation vs. Fe(3+) implicated in the Fenton reaction plays a major role in HO(·) deactivation process. Moreover, our results show that no saturation of the respective zeolite active sites occurred. This is possible only when ROS are actively converted to water molecules within the zeolite void system, which generates H(+) ion transport. Because zeolites cannot be administered in blood, their use in medicine should be limited to extra corporeal circuits. Zeolites could be of use during cardiopulmonary bypass or hemodialysis procedures.