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E Barreiro

Publications and source records attributed to E Barreiro.

At least 19 recordsLinked to original sources
PubMed2006

[Physiologic particularities of muscle impairments in the patient with COPD].

Patients with chronic obstructive pulmonary disease (COPD) frequently have skeletal muscle dysfunction, of either respiratory muscles or those located of the limbs. This dysfunction may appear even at relatively early stages and it conditions symptoms and patient's quality of life. In the case of respiratory muscles, factors that seem to determine muscle dysfunction are, particularly, changes in thorax configuration and an unbalance between decreased energy availability and increased energy demands by the muscle. However, respiratory muscles show signs of structural and metabolic adaptation to this situation, partially compensating the above-mentioned deleterious effects. However, at muscles of the limbs, particularly of the lower limbs, dysfunction seems to be essentially due to deconditioning by physical activity reduction. Structural changes in these muscles are involutional in nature. At both respiratory and peripheral muscles, other factors such as nutritional impairments, inflammation, oxidative stress, some drugs, and the presence of comorbidity seem to play a relevant role. All of them will condition both dysfunction and structural changes, which will be heterogeneous for the different muscle groups in each patient.

Humans↗
PubMed2005

Respiratory loading intensity and diaphragm oxidative stress: N-acetyl-cysteine effects.

We hypothesized that resistive breathing of moderate to high intensity might increase diaphragm oxidative stress, which could be partially attenuated by antioxidants. Our objective was to assess the levels of oxidative stress in the dog diaphragm after respiratory muscle training of a wide range of intensities and whether N-acetyl-cysteine (NAC) might act as an antioxidant. Twelve Beagle dogs were anesthetized with 1% propophol, tracheostomized, and subjected to continuous inspiratory resistive breathing (IRB) (2 h/day for 2 wk). They were further divided into two groups (n = 6): NAC group (oral NAC administration/24 h for 14 days) and control group (placebo). Diaphragm biopsies were obtained before (baseline biopsy) and after (contralateral hemidiaphragm) IRB and NAC vs. placebo treatment. Oxidative stress was evaluated in all diaphragm biopsies through determination of 3-nitrotyrosine immunoreactivity, protein carbonylation, hydroxynoneal protein adducts, Mn-SOD, and catalase, using immunoblotting and immunohistochemistry. Both protein tyrosine nitration and protein carbonylation were directly related to the amount of the respiratory loads, and NAC treatment abrogated this proportional rise in these two indexes of oxidative stress in response to increasing inspiratory loads. A post hoc analysis revealed that only the diaphragms of dogs subjected to high-intensity loads showed a significant increase in both protein tyrosine nitration and carbonylation, which were also significantly reduced by NAC treatment. These results suggest that high-intensity respiratory loading-induced oxidative stress may be neutralized by NAC treatment during IRB in the canine diaphragm.

Acetylcysteine↗
PubMed2005

N-acetylcysteine increases manganese superoxide dismutase activity in septic rat diaphragms.

The antioxidant N-acetylcysteine (NAC) prevented sepsis-induced diaphragmatic dysfunction. As an indirect antioxidant NAC was shown to induce superoxide dismutase (SOD) activity in immune cells from endotoxaemic mice. The aim of this study was to assess whether NAC acts as an indirect antioxidant by inducing manganese (Mn)-SOD activity in the diaphragms of endotoxaemic rats, while preventing muscle dysfunction. A controlled study was conducted, in which protein carbonylation, Mn-SOD, catalase, and 3-nitrotyrosine immunoreactivity were detected using immunoblotting and immunohistochemistry in rat diaphragms. Six groups were studied for 24 h after a saline (control) or lipopolysaccharide (LPS; 20 mg.kg-1) i.p. injection in the absence and presence of NAC pre-treatment (either 1.5 or 3 mmol.kg(-1).24 h-1 for 7 days, oral administration). Diaphragm mitochondrial Mn-SOD activity and respiratory muscle function were also determined. Within 24 h, LPS induced maximal inspiratory pressure reduction, increasing diaphragmatic protein carbonylation and nitration. Pre-treatment with 3 mmol.kg-1 NAC clearly increased muscle Mn-SOD protein content and activity in both LPS- and saline-injected animals, while reducing protein carbonylation and nitration, and partially preventing the LPS-induced respiratory muscle dysfunction. Data produced from this study indicate that high doses of N-acetylcysteine induces manganese superoxide dismutase, as well as preserves its activity, possibly by preventing nitration of critical tyrosine residues of the enzyme.

Acetylcysteine↗
PubMed2005

Time-based gene expression programme following diaphragm injury in a rat model.

It was hypothesised that diaphragm injury activates a time-based programme of gene expression in muscle repair. Gene expression of different substances, such as proteases (calpain 94 (p94)), transcription factors (myogenin and cFos), growth factors (both basic fibroblast growth factor (bFGF) and insulin-like growth factor (IGF)-II), and structural proteins (myosin heavy chain (MHC) and titin), was quantified by RT-PCR in rat diaphragms exposed to caffeine-induced injury. Injured and noninjured (control) rat hemidiaphragms were excised at different time points (1-240 h). In injured hemidiaphragms, in comparison with control muscles, p94 expression levels peaked at 1 h post-injury (PI), cFos mRNA levels began to rise, after an initial dip, and peaked at 96 h PI, while myogenin mRNA levels started to increase as early as 12 h PI, IGF-II mRNA levels initially decreased until 48 h PI and increased thereafter, peaking at 72 h PI, bFGF mRNA levels rose to a maximum at 96 h PI, and MHC and titin mRNA levels were significantly elevated at 72 h PI. Caffeine-induced diaphragm injury is followed by a time-based expression programme of different genes tailored to meet muscle repair needs.

Animals↗
PubMed2004

[Analysis of respiratory muscle structure and tumor necrosis and insulin-like growth factor expression in chronic obstructive pulmonary disease: are samples valid if obtained during thoracotomy performed because of localized pulmonary neoplasia?].

OBJECTIVE: Various methods have been used to obtain samples to study the structure of human respiratory muscles and the expression of diverse substances in them. Samples are most often obtained from autopsies, from muscle biopsies during thoracotomy performed because of a localized pulmonary lesion (TLL), and from ambulatory thoracoscopic biopsy in patients free of comorbidity (AT). The disadvantage of the first 2 of these methods lies in the possibility of interference from factors related to the patient's death in the first case or from the disease that necessitated surgery in the second. Although AT is free from the disadvantages of the other 2 methods, it is impossible to obtain samples of the diaphragm the principal respiratory muscle with this procedure. The objective of this study was to analyze the fibrous structure of the external intercostal muscle of patients with chronic obstructive pulmonary disease and to quantify the expression of the principal inflammatory cytokine tumor necrosis factor alpha (TNF-alpha)- and of insulin-like growth factor (IGF-1) in the same muscle, comparing the results obtained with TLL and AT samples. METHODS: Prospective and consecutive samples were taken of the external intercostal muscle (fifth space, anterior axillary line) in 15 patients with chronic obstructive pulmonary disease (mean [SD] age 66 [6] years; forced expiratory volume in 1 second 49% [9%] of predicted; PaO2 75 [9] mm Hg). Samples were taken during TLL (8 patients, all with pulmonary neoplasms but carefully selected in order to rule out systemic effects) or TA (7 patients). Patients with serious comorbidity were excluded from the second group. Samples were processed for structural analysis of fibers (immunohistochemical and enzymatic histochemical) and genetic expression of TNF-alpha and IGF-1 (real-time polymerase chain reaction). RESULTS: No differences in the structure of fibers were found between the 2 groups. No differences were observed in the expression of TNF-alpha or IGF-1. CONCLUSIONS: Using rigorous criteria, the TLL method appears to be suitable for studying the structural characteristics and expression of inflammatory cytokines and growth factors in the external intercostal muscle. Moreover, it can also be inferred that TLL is probably also useful for obtaining samples of the diaphragm, a muscle which cannot currently be sampled by any alternative method.

Aged↗
PubMed2004

Glutathione and glutamate levels in the diaphragm of patients with chronic obstructive pulmonary disease.

Recently, decreased glutamate (Glu) and reduced glutathione (GSH) levels were reported in the quadriceps femoris of patients with chronic obstructive pulmonary disease (COPD). The aim of the present study was to investigate whether Glu and GSH levels are also modified in the diaphragm of these patients. Nine male COPD patients (forced expiratory volume in one second (FEV1) range 28-68% of the predicted value) and seven male patients with normal pulmonary function (mean +/- SD FEV1 86 +/- 3% pred) submitted to thoracotomy were included. Biopsy specimens were taken from the diaphragm (both groups) and the quadriceps femoris (COPD group alone) in order to assess fibre size, myosin heavy chain expression, GSH levels and amino acid profile. The COPD group was characterised by preserved fibre size, a higher proportion of type I fibres (mean +/- SEM 70 +/- 3 versus 26 +/- 4%), and higher Glu and GSH content in the diaphragm compared to the quadriceps muscle. However, Glu and GSH levels were similar in diaphragm from the COPD and control groups. Glu level correlated with GSH level in both muscles. No significant correlation was found between Glu or GSH level and fibre size or proportions. This study shows that glutamate and reduced glutathione levels are preserved in the diaphragm of chronic obstructive pulmonary disease patients. Alterations in glutamate and reduced glutathione metabolism are muscle-specific in chronic obstructive pulmonary disease, affecting the quadriceps femoris but not the diaphragm. Glutamate and reduced glutathione levels are strongly interrelated in both muscles, independent of fibre type distribution and fibre size.

Aged↗
PubMed2004

Dyspnoea at rest and at the end of different exercises in patients with near-fatal asthma.

Blunted perception of dyspnoea under resistive loading has been observed in patients with a history of near-fatal asthma (NFA). The perception of dyspnoea at rest and at the end point of various exercises was assessed in such patients. Respiratory function and exercise capacity (6-min walking distance, incremental cycloergometry and inspiratory threshold loading) were assessed in seven NFA and eight non-NFA patients. Dyspnoea (Borg scale) was measured at rest and at the end point of the various exercises. Dyspnoea at rest was significantly lower in NFA patients. Although exercise tolerance was similarly reduced in both the NFA and non-NFA groups, dyspnoea at peak cycle exercise was significantly lower in the former (2.6+/-2 versus 6.1+/-3.8 (Borg scale; mean+/-SD)), who mainly (86%) stopped because of leg discomfort. A similar trend was observed in the 6-min walking distance and inspiratory threshold loading tests. Dyspnoea at peak exercise was the best indicator of the NFA condition, with a sensitivity of 100% and specificity of 63% for a Borg scale score of < or = 6. Perception of dyspnoea is blunted in near-fatal asthma patients at both rest and the end point of various forms of exercise. Dyspnoea at peak exercise is the best indicator of the near-fatal asthma condition.

Adolescent↗
PubMed2002

Expiratory muscle endurance in chronic obstructive pulmonary disease.

BACKGROUND: A reduction in expiratory muscle (ExM) endurance in patients with chronic obstructive pulmonary disease (COPD) may have clinically relevant implications. This study was carried out to evaluate ExM endurance in patients with COPD. METHODS: Twenty three patients with COPD (FEV(1) 35 (14)% predicted) and 14 matched controls were studied. ExM endurance was assessed using a method based on the use of an expiratory threshold valve which includes two steps. In step 1 the load is progressively increased (50 g every 2 minutes) until task failure is reached, and the pressure generated against the highest tolerated load is defined as the maximal expiratory sustainable pressure (Pthmax). In step 2 subjects breathe against a submaximal constant load (80% of Pthmax) and the time elapsed until task failure is termed the expiratory endurance time (Tth(80)). In addition, the strength of peripheral muscles (handgrip, HGS) and respiratory muscles (maximal inspiratory and expiratory pressures, PImax and PEmax, respectively) was evaluated. RESULTS: Patients with COPD had lower ExM strength and endurance than controls: PEmax 64 (19)% predicted v 84 (14)% predicted (mean difference 20%; 95% confidence intervals (CI) 14 to 39); Pthmax 52 (27) v 151 (46) cm H(2)O (mean difference 99, 95% CI 74 to 123); and Tth(80) 9.4 (6.3) v 14.2 (7.4) min (mean difference 4.8, 95% CI 1.0 to 10.4; p<0.01 for all). Interestingly, ExM endurance directly correlated with both the severity of airways obstruction (Pthmax with FEV(1), r=0.794, p<0.01) and the reduction in strength observed in different muscle groups (Pthmax with HG, PImax or PEmax, r=0.550, p<0.05; r=0.583, p<0.001; and r=0.584, p<0.001, respectively). CONCLUSIONS: ExM endurance is decreased in patients with COPD. This impairment is proportional to the severity of the disease and is associated with lower strength in different muscle groups. This suggests that systemic effects are implicated in the impairment observed in ExM function.

Electromyography↗
PubMed2001

Novel mutations and defective protein kinase C activation of T-lymphocytes in ataxia telangiectasia.

Three ataxia telangiectasia (AT) patients have been characterized immunologically and molecularly. Patient 1 presents two nondescribed splicing mutations which affect exons 15 and 21 of the ATM gene. The maternal defect consists of a G > A transition in the first nucleotide of the intron 21 donor splicing site which results in a complete deletion of exon 21. The paternal mutation consists of an A > C transversion in the intron 14 acceptor splicing site which produces a partial skipping of exon 15. Two abnormal alternative transcripts were found, respectively, 17 and 41 nucleotides shorter. Patient 2 presents a homozygous genomic deletion of 28 nucleotides in the last exon of the gene. This deletion changes the normal reading frame after residue 3003 of the protein and introduces a premature stop codon at residue 3008 that could originate a truncated ATM protein. Patient 3, a compound heterozygote, presents a defect which consists of a G > A transition in the first nucleotide of intron 62 donor splicing site which results in a complete deletion of exon 62. The results obtained during a three year period in the proliferation assays show an impaired PMA (phorbol myristate acetate) activation in specific T lymphocyte activation pathways (CD69, CD26, CD28, CD3, PHA, PWM and Con A mediated) but not in others (CD2, ionomycin, and Ig surface receptor). The possible link among specific ATM mutations and abnormal immune responses is unknown.

Ataxia Telangiectasia↗
PubMed2001

Morphological and functional recovery from diaphragm injury: an in vivo rat diaphragm injury model.

Our objective was to develop an in vivo model to study the timing and mechanisms underlying diaphragm injury and repair. Diaphragm injury was induced in anesthetized rats by the application of a 100 mM caffeine solution for a 10-min period to the right abdominal diaphragm surface. Diaphragms were removed 1, 4, 6, 12, 24, 48, 72, and 96 h and 10 days after the injury, with contractile function being assessed in strips in vitro by force-frequency curves. The extent of caffeine-induced membrane injury was indicated by the percentage of fibers with a fluorescent cytoplasm revealed by inward leakage of the procion orange dye. One hour after caffeine exposure, 32.9 +/- 3.1 (SE) % of fibers showed membrane injury that resulted in 70% loss of muscle force. Within 72-96 h, the percentage of fluorescent cells decreased to control values. Muscle force, however, was still reduced by 30%. Complete muscle strength recovery was observed 10 days after the injury. Whereas diaphragmatic fiber repair occurred within 4 days after injury induction, force recovery took up to 10 days. We suggest that the caffeine-damaged rat diaphragm is a useful model to study the timing and mechanisms of muscle injury and repair.

Animals↗
PubMed2001

Lipopolysaccharide-induced diaphragmatic contractile dysfunction and sarcolemmal injury in mice lacking the neuronal nitric oxide synthase.

In this study we evaluated the role of the neuronal nitric oxide synthase (nNOS) in lipopolysaccharide (LPS)-induced diaphragmatic contractile dysfunction and sarcolemmal injury. Wild-type (WT) mice or mice deficient in the nNOS gene (nNOS(-/-)) were injected with either saline (control) or Escherichia coli LPS (LPS groups) and sacrificed 12 h later. The diaphragm was then examined for NOS expression, NOS activity, and in-vitro contractility. We also assessed sarcolemmal injury in isolated muscle strips under resting condition and after 3 min of artificial stimulations. In WT mice, LPS injection reduced maximum force to about 75% of that of control animals and raised total NOS activity significantly due to the induction of the iNOS isoform. Although muscle fiber injury was minimal under resting condition, the percentage of injured fibers in control and LPS-injected mice approached 27% and 40% of total fibers, respectively, in response to artificial stimulation. By comparison, LPS injection in nNOS(-/-) mice elicited a worsening of muscle contractility (maximum force < 60% of control animals) but elicited degrees of sarcolemmal injury similar to those observed in the WT animals. In addition, muscle NOS activity and iNOS protein level in nNOS(-/-) mice injected with LPS reached about 10% and 60% of that of WT animals, respectively (p < 0.05 compared with WT animals). Protein level of endothelial NOS isoform in the diaphragm was not altered by LPS injection in either WT or nNOS(-/-) animals. We conclude that nNOS plays a protective role in attenuating the negative influence of sepsis on diaphragmatic contractility but is not involved in the pathogenesis of sepsis-induced sarcolemmal injury.

Animals↗
PubMed2001

Structural and functional changes in the skeletal muscles of COPD patients: the "compartments" theory.

This review focuses on the structural and functional changes occurring in respiratory as well as peripheral muscles in COPD patients. These changes are particular for each muscle territory or compartment. Respiratory muscles predominantly undergo structural adaptive changes. However, they have to do their job in unfavourable mechanical conditions and thus their function is impaired. Peripheral muscles have to be grouped in at least two different compartments: upper and lower limb muscles. The structure and function are relatively preserved in the former, due to the maintenance of some daily activities involving the arms or even the use of some of these muscles in the ventilatory effort. Lower limb muscles in contrast undergo involute structural changes which result in an impairment in their function and in the global exercise capacity of the individual. Deconditioning due to a reduction in daily activities secondary to ventilatory impairment is probably the driving factor for these changes. Although the level of activity appears to be the main determining factor in changes occurring in different territories, this would be modulated by other local and systemic factors, such as inflammation, oxidative stress, drugs and nutritional abnormalities.

Biopsy, Needle↗
PubMed2000

[Features of patients with bronchial asthma seen at the emergency department of a referral hospital in a semirural area].

UNLABELLED: Bronchial asthma is a chronic disease whose prevalence and severity is increasing. Appropriate treatment of exacerbation seems to affect the subsequent course of disease. OBJECTIVES: To assess the extent of application of guidelines for treating exacerbations of asthma and to describe the clinical and epidemiological characteristics of patients. PATIENTS AND METHODS: All patients presenting with exacerbations to the emergency room of a referral hospital in a semi-rural area of Catalonia were enrolled consecutively. We recorded symptoms, function and treatment variables during the emergency and when the patient was stable, at which time we also administered the Asthma Quality of Life Questionnaire (AQLQ). RESULTS: Forty-seven percent of patients resided in rural villages. Seventy-one percent lived in the area served by our hospital. Of the remaining patients, 57% came from municipalities in the Baix Empordà area, 29% in Alt Empordà area and 14% in La Selva area. Seventy-one percent went to the hospital directly from home, 66% of them were in the province of Girona; 75% of those homes were within urban areas. Of the 29% who had been sent to the emergency room by a physician, 71% were from a rural area. The 119 asthma exacerbations treated (114 patients, 71 females, 42 +/- 23 years) accounted for 0.3% of all emergency room visits. The exacerbation was considered severe in 31%, moderate in 47% and mild in all remaining cases. Eighty-eight percent of patients had experienced an exacerbation before. Symptoms were often present before the attack, but nearly half the patients were receiving relatively inadequate medication. Peak expiratory flow and oxygen saturation were recorded in 70% of cases and both variables improved after initial treatment (250 +/- 97 to 349 +/- 92 l/min, p < 0.001; and 92 +/- 7 to 96 +/- 2%, p < 0.01, respectively). All patients received inhaled salbutamol, 44% inhaled corticosteroids and 73% intravenous corticosteroids. A quarter of the patients were admitted to the ward (0.4% of all admissions) and 4% were admitted to the intensive care unit. Patients stayed 8.8 +/- 1.4 h in the emergency room. When patients were stable, asthma was severe in 14%, moderate in 42%, mild but persistent in 27%, and occasional in 17%. The total score on the AQLQ was 13.8 +/- 11.1, with mood being the dimension with the highest score (5.1 +/- 4.9). This score, along with social restriction, were lowest in the group of patients with chronic airflow obstruction. CONCLUSIONS: Nearly half the patients were from rural villages most of which were located outside the zone served directly by our hospital. The preference for specialized medical attention would explain the percentage of patients seen who did not belong to the assigned area. Difficulty of access to the hospital from certain rural areas would account for the greater number of rural patients who had been referred by a physician. Clinical management and monitoring of asthmatic patients with exacerbation could be improved by greater diffusion and application of guidelines. It would be interesting to incorporate come sort of questionnaire on quality of life while taking a patient's history.

Adolescent↗
PubMed2000

[The characteristics of the mechanical activity of the respiratory muscles during the diaphragmatic respiration technic].

UNLABELLED: Noteworthy among breathing training techniques is so-called diaphragmatic breathing. In spite of the technique's name, however, little is known of the functional characteristics of this ventilatory method. OBJECTIVE: To asses the mechanics of respiratory muscles, particularly diaphragm muscles, during diaphragmatic breathing in patients with severe chronic obstructive pulmonary disease (COPD). METHODS: Ventilatory pattern and respiratory pressures (abdominal [Pga], intrathoracic [Pes] and transdiaphragmatic [Pdi]) were studied in 10 patients with severe COPD in stable phase (age 69 +/- 6 years, FEV1 33 +/- 12% ref) at baseline and during deep breathing with spontaneous muscle recruitment (SMR) and during breathing training. Measurements were taken with the patient seated and in supine decubitus position. RESULTS: In seated position ventilatory pattern was similar with SMR and during breathing training. Mean Pdi during airflow, however, was greater during breathing training than with SMR (34.8 +/- 8.0 and 29.3 +/- 9.3 cmH2O, respectively, p < 0.05) for similar levels of Pes. Mechanical effectiveness of the diaphragm expressed as Vt/Pdi) was less during breathing training, however (36.1 +/- 10.4 and 49.5 +/- 15.8 cc/cmH2O, p < 0.05), with no changes in overall efficacy of respiratory muscles (Vt/Pes). In supine decubitus position, ventilatory patterns of SMR and breathing training were similar, although Vt and T1 were slightly higher in the latter (1,065 +/- 305 vs. 1,211 +/- 314 cc, p < 0.01; and 2.76 +/- 1.32 vs. 3.07 +/- 1.23 sec, p < 0.05). Pdi was also higher during breathing training (29.7 +/- 10.2 and 38.0 +/- 10.5 cmH2O, p < 0.05), although accompanied in this case by a higher Pes (21.2 +/- 7.5 to 26.4 +/- 8.4 cmH2O, p < 0.005). In supine decubitus position, the effectiveness of both diaphragm muscles and respiratory muscles overall was similar for both ventilatory modes. CONCLUSIONS: Breathing training truly involves greater use of the diaphragm, both in seated and supine decubitus positions. Breathing training does not provide greater ventilatory efficacy than SMR, however, in COPD patients.

Aged↗
PubMed2000

Patients hospitalized for COPD have a high prevalence of modifiable risk factors for exacerbation (EFRAM study).

There is little information available concerning the extent to which chronic obstructive pulmonarv disease (COPD) patients are satisfactorily managed, especially, regards factors supposedly related to COPD exacerbation. The present study assessed the prevalence rates of potentially modifiable risk factors of COPD exacerbation in patients hospitalized for this reason. A systematic sample of one out of two patients admitted for COPD exacerbation, during 1 yr, in four tertiary hospitals in the Barcelona area, Spain, was performed. Patients answered a questionnaire and underwent anthropometric measurements, spirometric tests and arterial blood gas sampling. Prevalence rates and 95% confidence intervals (95% CI) for risk factors were obtained, and the generalized estimating equation (GEE) method was used to allow for patients to provide information on different admissions. The study recruited 353 patients (29 female) with a total of 404 admissions age (mean+/-SD) 69+/-9, median forced expiratory volume in one second (FEV1) 31% of predicted and mean partial pressure of oxygen (PO2) 63+/-13 mmHg. Of these, 28% had not received an influenza vaccination; a high number (86%) did not attend rehabilitation programmes; 28% of patients with PO2 < or =55 mmHg were not using long-term oxygen therapy (LTOT); among LTOT users, 18% used it <15 h a day; 43% of the total failed in some of the essential inhaler manoeuvres; 26% were current smokers; 21% of noncurrent smokers were exposed to passive smoking at home; current occupational exposure was low (5%). In summary, the authors found a moderate to high prevalence of potentially modifiable risk factors in a large representative sample of patients hospitalized for a chronic obstructive pulmonary disease exacerbation, suggesting unsatisfactory features in their management.

Aged↗