Association of biomarkers with health-related quality of life and history of stressors in myalgic encephalomyelitis/chronic fatigue syndrome patients.

Background: Myalgic encephalomyelitis chronic fatigue syndrome (ME/CFS) is a common debilitating disorder associated with an intense fatigue, a reduced physical activity, and an impaired quality of life. There are no established biological markerof the syndrome. The etiology is unknown and its pathogenesis appears to be multifactorial.

Pathophysiological and diagnostic implications of cardiac biomarkers and antidiuretic hormone release in distinguishing immersion pulmonary edema from decompression sickness.

Immersion pulmonary edema (IPE) is a misdiagnosed environmental illness caused by water immersion, cold, and exertion. IPE occurs typically during SCUBA diving, snorkeling, and swimming. IPE is sometimes associated with myocardial injury and/or loss of consciousness in water, which may be fatal.

Effectiveness of pure argon for renal transplant preservation in a preclinical pig model of heterotopic autotransplantation.

Background: In kidney transplantation, the conditions of organ preservation following removal influence function recovery. Current static preservation procedures are generally based on immersion in a cold-storage solution used under atmospheric air (approximately 78 kPa N2, 21 kPa O2, 1 kPa Ar). Research on static cold-preservation solutions has stalled, and modifying the gas composition of the storage medium for improving preservation was considered.

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.

Genotoxicity of intraperitoneal injection of lipoamphiphile CdSe/ZnS quantum dots in rats.

The main objective of the present in vivo rat study was to determine the genotoxicity of lipoamphiphile-coated CdSe/ZnS Quantum Dots (QDs), in several organs (brain, liver, kidneys, lungs and testicles). The second objective was to establish the correlations between the QDs genotoxic activity and the oxidative stress, the production of a proinflammatory cytokine (TNF-α), a stress-induced chaperone protein, the phosphorylated heat shock protein 70 (pHsp70), and an increase in the caspase-3 apoptosis factor. Four QDs doses were injected into the peritoneal cavity (5, 5×10(-1), 5×10(-2) and 5×10(-3)μg/kg).

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.

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).

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.

Activation of nicotinic cholinergic receptors prevents ventilator-induced lung injury in rats.

Respiratory distress syndrome is responsible for 40 to 60 percent mortality. An over mortality of about 10 percent could result from additional lung injury and inflammation due to the life-support mechanical ventilation, which stretches the lung. It has been recently demonstrated, in vitro, that pharmacological activation of the alpha 7 nicotinic receptors (α7-nAChR) could down regulate intracellular mediators involved in lung cell inflammatory response to stretch.

Hyperoxia-induced alterations in cardiovascular function and autonomic control during return to normoxic breathing.

Hyperoxia causes hemodynamic alterations. We hypothesized that cardiovascular and autonomic control changes last beyond the end of hyperoxic period into normoxia. Ten healthy volunteers were randomized to breathe either medical air or 100% oxygen for 45 min in a double-blind study design.

Substance P receptor blockade decreases stretch-induced lung cytokines and lung injury in rats.

Overdistension of lung tissue during mechanical ventilation causes cytokine release, which may be facilitated by the autonomic nervous system. We used mechanical ventilation to cause lung injury in rats, and studied how cervical section of the vagus nerve, or substance P (SP) antagonism, affected the injury. The effects of 40 or 25 cmH(2)O high airway pressure injurious ventilation (HV(40) and HV(25)) were studied and compared with low airway pressure ventilation (LV) and spontaneous breathing (controls).

Combination of two oxidant stressors suppresses the oxidative stress and enhances the heat shock protein 27 response in healthy humans.

We tested the hypothesis that the combination of 2 oxidant stressors (hyperoxia and fatiguing exercise) might reduce or suppress the oxidative stress. We concomitantly measured the plasma concentration of heat shock proteins (Hsp) that protect the cells against the deleterious effects of reactive oxygen species. Healthy humans breathed pure oxygen under normobaric condition for 50-minute periods during which they stayed at rest or executed maximal static handgrip sustained until exhaustion.

Reactive oxygen species activate the group IV muscle afferents in resting and exercising muscle in rats.

We tested the hypothesis that the reactive oxygen species (ROS) produced at rest and mostly during muscle contraction may stimulate the group IV muscle afferents. In rats, afferent activity was recorded in the peroneal nerve innervating the tibialis anterior muscle. Group IV afferents were identified from measurements of their conduction velocity and response to lactic acid.

The changes in neuromuscular excitability with normobaric hyperoxia in humans.

Based on previous observations in hyperbaric hyperoxia, we hypothesized that normobaric hyperoxia, often used during general anaesthesia and resuscitation, might also induce a neuromuscular excitability. In healthy volunteers, we studied the consequences of a 50 min period of pure oxygen breathing on the neuromuscular conduction time (CT), the amplitude of the compound evoked muscle potential (M-wave), the latency and amplitude of the Hoffman reflex (H reflex) and the electromyographic tonic vibratory response (TVR) of the flexor digitorum superficialis muscle to explore the proprioceptive reflex loop. Hyperoxia-induced oxidative stress was measured by the changes in blood markers of lipid peroxidation (thiobarbituric acid reactive substances, TBARS) and antioxidant response (reduced ascorbic acid, RAA).

Reactive oxygen species and inflammatory mediators enhance muscle spindles mechanosensitivity in rats.

We tested the hypothesis that reactive oxygen species (ROS) and inflammatory mediators affect transduction properties of muscle spindles. In rats, muscle spindles response to high-frequency vibration (HFV) was recorded before and after (1) injection of hydrogen peroxide (H2O2) in control rats and animals pre-treated with diclofenac (anti-inflammatory substance), (2) injection of bradykinin and (3) fatigue induced by muscle stimulation (MS) in control rats and rats receiving diclofenac, superoxide dismutase (SOD) or H2O2. Muscular oxidative stress and inflammation induced by H2O2 or MS were assessed by measurements of isoprostanes and IL-6 levels.

Fatigue-induced changes in tonic vibration response (TVR) in humans: relationships between electromyographic and biochemical events.

Fatigue-induced changes in the proprioceptive reflex loop were explored in humans by using the tonic electromyographic (EMG) response to vibration (TVR) and relating it to lactic acidosis (LA) and oxidative stress. TVR was measured in flexor digitorum superficialis before and after sustained or intermittent handgrip at maximal voluntary contraction (MVC). TVR variations were compared with the changes in EMG power spectrum preceding contractile fatigue, the Hoffman reflex (H-reflex), and plasma concentrations of LA and thiobarbituric acid reactive substances (TBARS).

Enhanced exercise-induced plasma cytokine response and oxidative stress in COPD patients depend on blood oxygenation.

In healthy subjects, hypoxemia and exercise represent independent stressors promoting the exercise-induced cytokine response and oxidative stress. We hypothesized that hypoxemia in patients with chronic obstructive pulmonary disease (COPD) may affect the cytokine production and/or the changes in oxidant-antioxidant status in response to maximal exercise. Exercise-induced changes in PaO2 allowed to transiently increase or decrease baseline hypoxemia and to point out its specific action on muscle metabolism.

High-frequency percussive ventilation attenuates lung injury in a rabbit model of gastric juice aspiration.

Objective: To test the effects of high-frequency percussive ventilation (HFPV) compared with high-frequency oscillatory ventilation (HFOV) and low-volume conventional mechanical ventilation (LVCMV), on lung injury course in a gastric juice aspiration model.

Design: Prospective, randomized, controlled, in-vivo animal study.

Setting: University animal research laboratory.

Cytokine and oxidative responses to maximal cycling exercise in sedentary subjects.

Introduction: The simultaneous determination of the time course and magnitude of oxidative stress indicators and cytokine changes elicited by maximal incremental exercise has not yet been published for healthy sedentary subjects.

Purpose: The determination of normal exercise-induced changes in oxidant-antioxidant status and plasma cytokine represents a fundamental step before exploring patients suspected of altered biochemical responses.

Methods: Fifteen healthy sedentary subjects performed an incremental cycle exercise until volitional exhaustion with measurement of maximal oxygen uptake (VO2max), two cytokines (IL-6 and TNF-alpha), and three indicators of oxidative stress (plasma thiobarbituric acid reactive substances (TBARS), reduced erythrocyte glutathione (GSH), and reduced plasma ascorbic acid (RAA)).

Physiological, histological and biochemical properties of rat skeletal muscles in response to hindlimb suspension.

In previous study, we found that the reduced exercise-induced production of reactive oxygen species (ROS) reported in slow-oxidative muscle of hypoxemic rats and also in chronic hypoxemic patients did not simply result from deconditioning. In control rats and after a 3-week period of hindlimb suspension (HS), the slow-oxidative (Soleus, SOL) and fast-glycolytic skeletal muscles (Extensor digitorum longus, EDL) were sampled. We determined the response to direct muscle stimulation (twitch stimulation (TS), Maximal force (Fmax)), twitch amplitude and maximal relaxation rate, tetanic frequency, endurance to fatigue after muscle stimulation (MS), the different fibre types based on their myofibrillar adenosinetriphosphatase (ATPase) activity, and the intra-muscular redox status (Thiobarbituric Acid Reactive Sustances: TBARS, reduced glutathione: GSH, reduced ascorbic acid: RAA).

Reliability of different blood indices to explore the oxidative stress in response to maximal cycling and static exercises.

This study compares the changes in four blood markers of exercise-induced oxidative stress in response to exercise protocols commonly used to explore the global muscle performance at work (maximal incremental cycle) and endurance to fatigue of selected muscles (static handgrip and thumb adduction). Cycling and static exercises allow the muscle to work in aerobic and anaerobic conditions, respectively. Healthy adults performed an incremental cycling exercise until volitional exhaustion and, on separated days, executed infra-maximal static thumb adduction and handgrip until exhaustion.

The oxidative stress in response to routine incremental cycling exercise in healthy sedentary subjects.

The kinetics of blood markers of the oxidative stress during and after an incremental exercise until the maximal performances is not documented in healthy sedentary subjects. We studied subjects of both sexes cycling on an ergometer until or near the V(O)(2)(max) measurement, and we measured during exercise and a 30-min recovery period the plasma concentration of thiobarbituric acid reactive substances (TBARS) which explored the production of reactive oxygen species (ROS) and two antioxidants (plasma reduced ascorbic acid (RAA) and erythrocyte reduced glutathione (GSH)). Despite we noted inter-individual differences in the instants of maximal variations of TBARS, GSH, and RAA, they were all measured within the first 20 min of the post-exercise recovery period, and at the 30th min of recovery, the three ROS blood markers tended to recover their pre-exercise levels.

Depressed fatigue-induced oxidative stress in chronic hypoxemic humans and rats.

It was already documented that acute hypoxemia reduces the oxidative stress following static as well as dynamic handgrip bouts in humans. Then, we examined if chronic hypoxemia could produce the same effect in patients suffering from chronic respiratory insufficiency. In rats, we studied the respective consequence of a one-month exposure to normobaric hypoxia on two muscles (soleus, SOL, and extensor digitorum longus, EDL) which have high and low aerobic metabolism, respectively.

Influence of chronic hypoxemia on peripheral muscle function and oxidative stress in humans.

Transient re-oxygenation of humans suffering from chronic obstructive pulmonary disease (COPD) allows the assessment of the consequences of chronic hypoxemia on peripheral muscle and metabolism apart from the effects of de-conditioning. The subjects performed maximal voluntary contractions (MVC) of flexor digitorum and vastus lateralis muscles and sustained infra-maximal contractions. COPD patients repeated the whole challenge during a 50-min oxygen breathing period and after recovery to baseline hypoxemia.